DETAILED ACTION Notice of Pre-AIA or AIA Status The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA. Information Disclosure Statement The information disclosure statement (IDS) submitted on 10/23/2023 and 10/19/2023 were filed in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner. Claim Interpretation Claim 24 recites a method of treating lung injury , wherein the lung injury is caused by an increase in neutrophils; and/or wherein the lung injury is caused by a cytokine storm. Here, the term “caused by” is unclear . It is recognized in the art that c ytokine storms and increased neutrophils are fairly directly caused by many different immune triggers ( like the presence and detection of pathogens ) , which are typically referred to as the “causes” of immune response-associated injury. Under the broadest reasonable interpretation of “caused by,” the term will be interpreted as meaning “associated with.” For example, in the context of claim 24, the claim will be interpreted as the method of claim 21 wherein the lung injury is associated with an increase in neutrophils; and/or wherein the lung injury is associated with a cytokine storm. Moreover, for clarity of the record and because it is not clearly defined otherwise in the specification, the term “cytokine storm” will be interpreted as a severe immune reaction in which the body releases a n abnormally high number of cytokines into the blood or another tissue quickly. This is because the term “cytokine storm” does not have a clear threshold for classification as such. Claim Rejections - 35 USC § 112 The following is a quotation of the first paragraph of 35 U.S.C. 112(a): (a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention. The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112: The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention. Claim s 21-40 rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA), first paragraph, because the specification, while being enabling for treating or preventing pulmonary inflammation and inflammation-associated injury in acute respiratory distress syndrome with annexin A5 at 1 mg/kg , does not reasonably provide enablement for preventing any lung injury . The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make or use the invention commensurate in scope with these claims. In order to determine compliance with the enablement requirement of 35 U.S.C. 112(a), the Federal Circuit developed a framework of factors in In re Wands, 858 F.2d 731, 737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988), referred to as the Wands factors to assess whether any necessary experimentation required by the specification is "reasonable" or is "undue." Consistent with Amgen Inc. et al. v. Sanofi et al., 598 U.S. 594, 2023 USPQ2d 602 (2023), the Wands factors continue to provide a framework for assessing enablement in a utility application or patent, regardless of technology area. See Guidelines for Assessing Enablement in Utility Applications and Patents in View of the Supreme Court Decision in Amgen Inc. et al. v. Sanofi et al., 89 FR 1563 (January 10, 2024). These factors include, but are not limited to: (A) The breadth of the claims; (B) The nature of the invention; (C) The state of the prior art; (D) The level of one of ordinary skill; (E) The level of predictability in the art; (F) The amount of direction provided by the inventor; (G) The existence of working examples; and (H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure. With regard to the breadth of the invention, nature of the invention, and the state of the prior art, the invention is drawn to a method of treating or preventing injuries associated with inflammatory responses, and the nature of the invention is a method of treating lung injury with protein-based therapeutic. Here, the scope of the claims includes treating or preventing any lung injury, but the state of the prior art does not show that annexin therapeutics (or protein therapeutics, broadly) are capable of preventing any lung injury. Trivially, there is no indication in the prior art that blunt trauma, penetrating trauma, and crush injuries can be prevented by administering a protein therapeutic, but the broad scope of the claims include these injuries. As such, a person having ordinary skill in the art would not be enabled to make or use the invention commensurate with the scope. As in the example above, a person having ordinary skill in the art would not reasonably be enabled to prevent penetrating lung trauma in a subject by administering annexin to the subject according to the method of any one of claims 21-40, seeing as this is not recognized as possible in the art. With regard to the level of one of ordinary skill and the level of predictability in the art, one having ordinary skill in the art would not reasonably be enabled to make or use any protein therapeutic capable of preventing blunt, penetrating, or crush injuries to the lungs, as anti-inflammatory protein therapeutics have predictable functions in the art that are orthogonal to preventing these types of traumas from occurring. With regard to the amount of direction provided by the inventor, the existence of working examples, and the quantity of experimentation needed to make or use the invention based on the content of the disclosure, Applicant has not provided any examples of entirely preventing any lung injury. Given that there are no examples or directions drawn to preventing lung injury, a person having ordinary skill in the art would not reasonably be enabled to make or use the invention commensurate with the scope of preventing all lung injuries. In other words, it would require extensive experimentation to prevent all lung injuries using the invention of the instant application, particularly considering that this is not recognized as possible in the art. Moreover, Applicant only provides examples of treating lung injuries with annexin A5 at 1 mg/kg dosage, rather than with any annexin protein at any dosage between 0.2 mg/kg to 5 mg/kg. Given that there is no direction and there are no disclosed examples of treating lung injuries with any annexins other than annexin A5, it has not been demonstrated that these annexins are capable of treating lung injury. It is advised that applicant amend the claims to reflect the embodiments of the invention that enable a person having ordinary skill in the art to make and use the invention commensurate with the scope. Specifically, Applicant is enabled for treating and/or preventing pulmonary inflammation and inflammation-associated injury in acute respiratory distress syndrome with annexin A5 . Claim Rejections - 35 USC § 102 In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis ( i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status. The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action: A person shall be entitled to a patent unless – (a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale , or otherwise available to the public before the effective filing date of the claimed invention. (a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention. Claims 21-40 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Hashimoto et al. ( filed on the IDS submitted 10/19/2023 , Hashimoto, Kohei et al. “Annexin V homodimer protects against ischemia reperfusion-induced acute lung injury in lung transplantation.” The Journal of thoracic and cardiovascular surgery vol. 151,3 (2016): 861-869 ) , as evidenced by Laubach et al. ( Laubach, Victor E, and Irving L Kron. “Pulmonary inflammation after lung transplantation.” Surgery vol. 146,1 (2009): 1-4 ) and Zheng et al. ( Zheng, Zhikun et al. “Donor pulmonary intravascular nonclassical monocytes recruit recipient neutrophils and mediate primary lung allograft dysfunction.” Science translational medicine vol. 9,394 (2017) ) . With regard to claim 21, Hashimoto et al. teach a method of treating acute lung injury comprising administering recombinant annexin V ( diannexin ) at a dose of 1 mg/kg to a subject, wherein the subject is a rat, a non-human mammal (see Title, page 862, paragraphs 2, 7 ). With regard to claim 22, Hashimoto et al. teach the method discussed above wherein the annexin is annexin V (see page 862, paragraph 2 ). With regard to claim 23, Hashimoto et al. teach the method discussed above wherein the lung injury is acute lung injury (see Title). With regard to claim 24, Hashimoto et al. teach the method discussed above wherein the acute lung injury is associated with a lung transplantation (see Title ). Moreover, as taught by Laubach et al., neutrophil activation is a key response to lung injury, including lung transplant (see page 2, paragraph 3). Specifically, neutrophils are activated and infiltrate damaged lungs upon lung injury like the lung transplant of Hashimoto et al. (see page 2, paragraph 3). As such, lung transplant s like that of Hashimoto et al. are associated with an increase in neutrophils that cause damage or injury in the lung. Similarly, Hashimoto et al. don’t explicitly teach that the treated lung injury is associated with increased cytokines, but, according to Laubach et al., the production of pro-inflammatory cytokines is increased considerably in the lung after transplantation (see page 2, paragraph 1). As such, the method of Hashimoto et al. is associated with a considerable increase in cytokines in the subject to be treated for lung injury. Here, there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference (Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003)). See also Toro Co. v. Deere & Co., 355 F.3d 1313, 1320, 69 USPQ2d 1584, 1590 (Fed. Cir. 2004), wherein "[T]he fact that a characteristic is a necessary feature or result of a prior-art embodiment (that is itself sufficiently described and enabled) is enough for inherent anticipation, even if that fact was unknown at the time of the prior invention." With regard to claim 25, Hashimoto et al. teach the method discussed above wherein the lung injury is associated with activation and infiltration of neutrophils into damaged post-transplant lung (see Hashimoto et al. Title) tissue, as evidenced by Laubach et al. (see Laubach et al. page 2, paragraph 3). Here, this represents a feature that was inherent in the disclosure, even though it was not recognized at the time. With regard to claim 26, Hashimoto et al. teach the method discussed above wherein the lung injury is associated with inflammatory cytokines (see Figure 4, page 865, paragraph 2). As discussed above, the term “cytokine storm” is interpreted as meaning an abnormally high number of cytokines released into a tissue. Hashimoto et al. don’t explicitly teach that the treated lung injury is associated with increased cytokines, but, according to Laubach et al., the production of pro-inflammatory cytokines is increased considerably in the lung after transplantation (see page 2, paragraph 1). As such, the method of Hashimoto et al. is associated with a considerable increase in cytokines in the subject to be treated for lung injury. Again, this represents a feature that was inherent in the disclosure, even though it was not recognized at the time. With regard to claim 27, Hashimoto et al. teach the method discussed above wherein the method reduces the inflammatory factors in the lungs (see page 895, paragraph 2 ). Specifically, they found lower interleukin-6, interleukin-1ß, and macrophage inflammatory protein 2 in terms of mRNA expression, with IL-6 lower in protein assays (see page 895, paragraph 2). With regard to claim 28, Hashimoto et al. teach the method discussed above, and they teach prior administration to humans (see page 867, paragraph 6). They do not, however, explicitly teach that the content of neutrophils in the subject to be treated (A1) is higher than the content in a normal subject (A0) at a ratio of A1/A0 is greater than or equal to 1.1. Regardless, Hashimoto et al. teach a method of treating lung transplantation with annexin A5 at 1 mg/kg, and according to Zheng et al., subjects with lung injury associated with lung transplantation have a content of neutrophils higher than a normal subject at a ratio greater than A1/A0 is equal to 1.1 (see Figure 8B ). Given that the increase in neutrophil content is a known feature of lung transplantation, the treatment of patients with said increase constitutes a previously unappreciated feature of the invention of Hashimoto et al. Here, as discussed above, there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference (Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003)). See also Toro Co. v. Deere & Co., 355 F.3d 1313, 1320, 69 USPQ2d 1584, 1590 (Fed. Cir. 2004), wherein "[T]he fact that a characteristic is a necessary feature or result of a prior-art embodiment (that is itself sufficiently described and enabled) is enough for inherent anticipation, even if that fact was unknown at the time of the prior invention." As such, given the fact that Hashimoto et al. teach treating a disease clearly associated with a statistically significant increase in neutrophil content at a ratio greater than A1/A0 is equal to 1.1, they anticipate this limitation. With regard to claim 29, Hashimoto et al. teach the method discussed above wherein the method reduces the pulmonary inflammatory factors (see page 895, paragraph 2). Specifically, they found lower interleukin-6 and macrophage inflammatory protein 2 in terms of mRNA expression (see page 895, paragraph 2). Moreover, as discussed above, lung transplantations like that of Hashimoto et al. are associated with increases in neutrophils in the lungs , as evidenced by Laubach et al. (see Laubach et al. page 2, paragraph 3). Given that Hashimoto et al. teach the same method of administering 1 mg/kg of annexin A5 to a subject with an acute lung injury, the method of Hashimoto et al. necessarily serves the same function as the method of claim 29. In other words, if administering annexin A5 at 1mg/kg is capable of reducing pulmonary inflammatory facts, reducing pulmonary white blood cells, and/or reducing pulmonary total proteins in the instant application, it is necessarily capable of doing so in the invention of Hashimoto et al. In the instant case, seeing as the invention of Hashimoto et al. uses the same chemical structure within the claimed dosage range to treat lung injury, it is inherently capable of achieving the claimed benefits of reducing inflammatory factors, reducing white blood cells, and reducing total pulmonary proteins in the lungs. Beyond this, t here is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference ( Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003) ). S ee also Toro Co. v. Deere & Co., 355 F.3d 1313, 1320, 69 USPQ2d 1584, 1590 (Fed. Cir. 2004) , wherein "[T]he fact that a characteristic is a necessary feature or result of a prior-art embodiment (that is itself sufficiently described and enabled) is enough for inherent anticipation, even if that fact was unknown at the time of the prior invention." Here, whether the inventors of Hashimoto et al. explicitly teach the reduction of certain inflammatory factors or leukocytes is irrelevant to the question of whether the method is capable of doing so. With regard to claim 30, Hashimoto et al. teach the method discussed above wherein the reduced inflammatory factors comprise interleukin-6 (see page 895, paragraph 2). Regardless, as discussed above, the invention of Hashimoto et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. As such, it is inherently capable of reducing the pulmonary inflammatory factors TNF-α, IL-10, IL-6, and/or IL-1ß , and this represents an inherent feature in the disclosure. With regard to claim 31, Hashimoto et al. teach the method discussed above wherein the method reduces the pulmonary inflammatory factors (see page 895, paragraph 2). Specifically, they found lower interleukin-6 and macrophage inflammatory protein 2 in terms of mRNA expression (see page 895, paragraph 2). They do not explicitly teach that the method reduces white blood cells, neutrophils, and monocytes. Here, Laubach et al. teach that lung transplantations like that of Hashimoto et al. involve neutrophils (see page 2, paragraph 3, lymphocytes (see page 3, paragraph 2 ), and monocytes (see page 4, paragraph 2 ), which are all species of white blood cells. Given that Hashimoto et al. teach administering annexin A5 at 1mg/kg, which is within the range claimed by the instant application, it is inherently capable of functioning in the same manner as claimed in the instant application, as discussed above. As such, given that it is the same protein administered at a claimed dosage, the inventions have the same structure and therefore the same function in reducing white blood cells, neutrophils, and monocytes. Again, this represents an inherent feature in the disclosure. With regard to claim 32, Hashimoto et al. teach the method discussed above wherein the method reduces the pulmonary inflammatory factors (see page 895, paragraph 2). Specifically, they found lower interleukin-6 and macrophage inflammatory protein 2 in terms of mRNA expression (see page 895, paragraph 2). This is measured as compared to a control group with the same lung injury absent the treatment. The reference doesn’t explicitly state that the E0/E1 is greater than 10, but, as discussed above, Hashimoto et al. teach administering the same composition as the instant application within the claimed dosage. As such, the composition of Hashimoto et al. inherently has the same structure and function as that of the instant application, including an ability to reduce pulmonary inflammatory factors of an administrated subject (E1) to a lower quantity than that of a control lung injury subject (E0) such that E0/E1 is greater than or equal to 10. Again, this represents an inherent feature in the disclosure , whether it was recognized at the time of disclosure or not . With regard to claim 33, Hashimoto et al. teach the method discussed above wherein the method reduces the pulmonary inflammatory factors (see page 895, paragraph 2). Specifically, they found lower interleukin-6 and macrophage inflammatory protein 2 in terms of mRNA expression (see page 895, paragraph 2). They do not explicitly teach that the method reduces white blood cells, neutrophils, and monocytes. Here, Laubach et al. teach that lung transplantations like that of Hashimoto et al. involve increases and activations of white blood cells (see page 2, paragraph 3, p age 3, paragraph 2 , and page 4, paragraph 2). Given that Hashimoto et al. teach administering annexin A5 at 1mg/kg, which is within the range claimed by the instant application, it is inherently capable of functioning in the same manner as claimed in the instant application, as discussed above. As such, given that it is the same protein administered at a claimed dosage, the inventions have the same structure and therefore the same function in reducing white blood cells as claimed in claim 33 of the instant application. Again, this represents an inherent feature in the disclosure , whether it was recognized at the time of disclosure or not . With regard to claim 34, Hashimoto et al. teach the method discussed above wherein the method reduces the pulmonary inflammatory factors (see page 895, paragraph 2). Specifically, they found lower interleukin-6 and macrophage inflammatory protein 2 in terms of mRNA expression (see page 895, paragraph 2). They do not explicitly teach that the method reduces pulmonary total proteins, but, as discussed above, they do teach administering the same chemical composition as the instant application within the claimed dosage range. As such, as recited above, it is inherently capable of reducing the total proteins, as claimed in claim 34. Again, this represents an inherent feature in the disclosure , whether it was recognized at the time of disclosure or not . With regard to claim 35, Hashimoto et al. teach the method discussed above wherein the method reduces the pulmonary inflammatory factors (see page 895, paragraph 2). Specifically, they found lower interleukin-6 and macrophage inflammatory protein 2 in terms of mRNA expression (see page 895, paragraph 2). With regard to claim 36, Hashimoto et al. teach the method discussed above wherein the method reduces the pulmonary inflammatory factors (see page 895, paragraph 2). Specifically, they found lower interleukin-6 and macrophage inflammatory protein 2 in terms of mRNA expression (see page 895, paragraph 2). Although Hashimoto et al. do not, as discussed above, teach that the method reduces inflammatory factors in serum within the claimed ratio of J0/J1 is greater than or equal to 20, they teach the administration of the same chemical compound, annexin A5, within the claimed dosage range. As such, the method of Hashimoto et al. inherently teaches administering a compound capable of achieving the results discussed in claim 36 of the instant application. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 37, Hashimoto et al. teach the method discussed above wherein methylprednisone sodium succinate is systemically administered in addition to annexin A5 (see page 862, paragraph 6). With regard to claim 38, Hashimoto et al. teach the method discussed above wherein the annexin is in a dosage form in the form of an injection into the jugular vein (see page 862, paragraph 7). With regard to claim 39, Hashimoto et al. teach the method discussed above wherein the annexin is in a dosage form in the form of an injection into the jugular vein (see page 862, paragraph 7). With regard to claim 40, Hashimoto et al. teach the method discussed above wherein the annexin is in a dosage form in the form of an injection into the jugular vein (see page 862, paragraph 7). Claim s 21-40 are rejected under 35 U.S.C. 10 2(a)(1) as being anticipated WO 2020132647 A1 , hereinafter Demonbreun et al. (as filed on the IDS submitted 10/23/2023, published 06/25/2020) , as evidenced by Pelaia et al. ( Pelaia , Corrado et al. “Lung under attack by COVID-19-induced cytokine storm: pathogenic mechanisms and therapeutic implications.” Therapeutic advances in respiratory disease vol. 14 (2020) ) and Zhu et al. ( Zhu, Zhe et al. “Clinical value of immune-inflammatory parameters to assess the severity of coronavirus disease 2019.” International journal of infectious diseases: IJID: official publication of the International Society for Infectious Diseases vol. 95 (2020): 332-339 ). With regard to claim 2 1, Demonbreun et al. teach a method for treating lung injury comprising administering annexin at a dose of about 1 mg/kg, 1 .5 mg/kg, 2 mg/kg, 2.3 mg/kg, 2.5 mg/kg, 3 mg/kg, 3.5 mg/kg, 4 mg/kg, 4.5 mg/kg, 5 mg/kg, 5.5 mg/kg, 6 mg/kg, 6.5 mg/kg, 7 mg/kg, 8 mg/kg, 9 mg/kg, or 10 mg/kg to a subject (see [0008] , [0168] ). They also teach that the dosage can be from 10 pg /kg up to about 20 mg/kg (see [0168]) and that the subjects can be humans or non-human mammals (see [0168]). With regard to claim 2 2, Demonbreun et al. teach the method discussed above wherein the annexin can be annexin A5 (see [0012], [0065], [0105] , [0106], [0107], and claims 20, 27). With regard to claim 23, Demonbreun et al. teach the method discussed above wherein the lung injury is acute lung injury (see claim 8, [0008], [0075]). With regard to claim 24, Demonbreun et al. teach the method discussed above wherein the lung injury can be associated with severe acute respiratory syndrome (SARS) (see [0075]). According to Pelaia et al., SARS is associated with cytokine storms and increases in neutrophils in lung injuries (see Figure 1). As such, the method of Demonbreun et al. is associated with a considerable increase in cytokines in the subject to be treated for lung injury. Here, there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference (Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003)). See also Toro Co. v. Deere & Co., 355 F.3d 1313, 1320, 69 USPQ2d 1584, 1590 (Fed. Cir. 2004), wherein "[T]he fact that a characteristic is a necessary feature or result of a prior-art embodiment (that is itself sufficiently described and enabled) is enough for inherent anticipation, even if that fact was unknown at the time of the prior invention." This represents a feature that was inherent in the disclosure of Demonbreun et al., regardless of whether it was explicitly taught. With regard to claim 25, Demonbreun et al. teach the method discussed above wherein the lung injury can be associated with severe acute respiratory syndrome (SARS) (see [0075]). According to Pelaia et al., SARS is associated with cytokine storms and increases in neutrophils in lung injuries (see Figure 1). Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 26, Demonbreun et al. teach the method discussed above wherein the lung injury can be associated with severe acute respiratory syndrome (SARS) (see [0075]). According to Pelaia et al. , SARS is associated with cytokine storms and increases in neutrophils in lung injuries (see Figure 1 ). Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 27, Demonbreun et al. teach the method discussed above wherein annexin is administered to treat lung injury (see claim 8, [0008], [0075]), and they teach that a nnexins have been shown to have anti-inflammatory, pro-fibrinolytic, and anti-thrombotic effects (see [0053]) . With regard to claim 28, Demonbreun et al. teach the method discussed above wherein annexin is administered to treat lung injury (see claim 8, [0008], [0075]) , but they do not explicitly teach that the human subject to be treated has a neutrophil content according to the claimed ratio of A1/A0. They do, however, teach the method discussed above wherein the lung injury can be associated with severe acute respiratory syndrome (SARS) (see [0075]). According to Zhu et al. , SARS is associated with increased neutrophils in lung injuries according to the ratio of A1/A0 is greater than or equal to 1.1 (see Table 2 ). Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 29, g iven that Demonbreun et al. teach the same method of administering annexin A5 at, for example, 5 mg/kg to a subject with an acute lung injury, the method of Demonbreun et al. necessarily serves the same function as the method of claim 29. In other words, if administering annexin A5 at 1mg/kg is capable of reducing pulmonary inflammatory facts, reducing pulmonary white blood cells, and/or reducing pulmonary total proteins in the instant application, it is necessarily capable of doing so in the invention of Demonbreun et al. This is on account of the fact that "products of identical chemical composition cannot have mutually exclusive properties" (In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990)). A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the properties applicant discloses and/or claims are necessarily present. In the case cited above, Applicant argued that the claimed composition was a pressure sensitive adhesive containing a tacky polymer while the product of the reference was hard and abrasion resistant. "The Board correctly found that the virtual identity of monomers and procedures sufficed to support a prima facie case of unpatentability of Spada’s polymer latexes for lack of novelty." In the instant case, seeing as the invention of Demonbreun et al. uses the same chemical structure within the claimed dosage range to treat lung injury, it is inherently capable of achieving the claimed benefits of reducing inflammatory factors, reducing white blood cells, and reducing total pulmonary proteins in the lungs. Beyond this, there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference (Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003)). See also Toro Co. v. Deere & Co., 355 F.3d 1313, 1320, 69 USPQ2d 1584, 1590 (Fed. Cir. 2004), wherein "[T]he fact that a characteristic is a necessary feature or result of a prior-art embodiment (that is itself sufficiently described and enabled) is enough for inherent anticipation, even if that fact was unknown at the time of the prior invention." Here, whether the inventors of Demonbreun et al. explicitly teach the reduction of certain inflammatory factors or leukocytes is irrelevant to the question of whether the method is inherently capable of doing so. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 30, as discussed above, the invention of Demonbreun et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. As such, it is inherently capable of reducing the pulmonary inflammatory factors TNF-α, IL-10, IL-6, and/or IL-1ß. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 31, Demonbreun et al. teach the method discussed above, but they do not explicitly teach reducing pulmonary white blood cells, neutrophils, lymphocytes, and monocytes. A s discussed above, the invention of Demonbreun et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 32, Demonbreun et al. teach the method discussed above, but they do not explicitly teach a lowering in the quantity of pulmonary factors (E1) of an administered subject as compared to a lung injury subject (E0) at a ratio of E0/E1 is greater than or equal to 10 . As discussed above, the invention of Demonbreun et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 33, Demonbreun et al. teach the method discussed above, but they do not explicitly teach a reduction in white blood cells of the administered subject (F1) as compared to a lung injury subject (F0) at a ratio of F0/F1 is greater than or equal to 3 . As discussed above, the invention of Demonbreun et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 34, Demonbreun et al. teach the method discussed above, but they do not explicitly teach a reduction of total pulmonary proteins (H1) of the administered subject as compared to that of a lung injury subject at a ratio of H0/H1 is greater than or equal to 2 . As discussed above, the invention of Demonbreun et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 35, Demonbreun et al. teach the method discussed above, but they do not explicitly teach reducing the inflammatory factors TNF-α, IL-10, IL-6, and/or IL-1ß . As discussed above, the invention of Demonbreun et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 36, Demonbreun et al. teach the method discussed above, but they do not explicitly teach reducing inflammatory factors in the serum of an administered subject (J1) as compared to a lung injury subject (J0) at a ratio of J0/J1 is greater than or equal to 20 . As discussed above, the invention of Demonbreun et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 37, Demonbreun et al. teach the method discussed above wherein the method can include an additional medication, which can be a glucocorticoid (see [0012] ). With regard to claim 38, Demonbreun et al. teach the method discussed above wherein the annexin is in an injection form (see [0026] -[0029]). With regard to claim 39, Demonbreun et al. teach the method discussed above wherein the injection is a systemic injection in the muscle, specifically myofibers (see [0026]). With regard to claim 40, Demonbreun et al. teach the method discussed above wherein the injection is a systemic injection in the muscle, specifically myofibers (see [0026]). Claim s 21- 36 and 38-40 are rejected under 35 U.S.C. 102(a)(1) and 102 (a)(2) as being anticipated by US 20200262866 A1 , hereinafter Maks et al. , as evidenced by Ray et al. ( Ray, Anuradha, and Jay K Kolls . “Neutrophilic Inflammation in Asthma and Association with Disease Severity.” Trends in immunology vol. 38,12 (2017): 942-954 ). With regard to claim 21, Maks et al. teach a method of administering to a human or animal in need thereof a therapeutically effective amount of annexin A5 (AnxA5) protein (see [0039], [0040]). They also teach that the method can be used to treat lung disorder (see [0381]), and they teach that a therapeutically effective amount of an AnxA5 protein can be, for example, greater than 0.1 mg/kg and up to or less than 20, 10, 5, 4, 3 or 2 mg/kg, such as about 1 mg/kg (see [0261]). With regard to claim 22, Maks et al. teach the method discussed above wherein the annexin is annexin A% ( AnxA5 ) (see [0039] and [0040]). With regard to claim 24, Maks et al. teach the method discussed above wherein the lung injury can be an allergic lung disorder, including asthma, allergic bronchopulmonary aspergillosis, or hypersensitivity pneumonitis (see [0371]). According to Ray et al. , asthma is associated with increased neutrophils in the sputum, the mucous of the airways and lungs (see page 3, paragraph 3 and page 4, paragraph 1). Here , as discussed above, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 25, Maks et al. teach the method discussed above wherein the lung injury can be an allergic lung disorder, including asthma, allergic bronchopulmonary aspergillosis, or hypersensitivity pneumonitis (see [0371]). According to Ray et al., asthma is associated with increased neutrophils in the sputum, the mucous of the airways and lungs (see page 3, paragraph 3 and page 4, paragraph 1). Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 26, Maks et al. teach the method discussed above wherein the lung injury can be an allergic lung disorder, including asthma, allergic bronchopulmonary aspergillosis, or hypersensitivity pneumonitis (see [0371]). According to Ray et al., asthma is associated with increased cytokine markers in the sputum, including IL-17, IL-8, and more (see page 3, paragraph 1). Moreover, they found that elevated neutrophils in the sputum was associated with elevated cytokines (see page 4, paragraph 1, page 6, paragraph 1). As discussed above, the term “cytokine storm” is interpreted as meaning an abnormally high number of cytokines released into a tissue. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 27, Maks et al. teach the method discussed above wherein the method is drawn to treating lung disorders, as recited above, and the method reduces inflammation (see [0367] and [0371]). With regard to claim 28, Maks et al. teach the method discussed above wherein the lung injury can be an allergic lung disorder, including asthma, allergic bronchopulmonary aspergillosis, or hypersensitivity pneumonitis (see [0371]). According to Ray et al., asthma is associated with increased neutrophils in the sputum, the mucous of the airways and lungs (see page 3, paragraph 3 and page 4, paragraph 1). Further according to Ray et al., t he percentage of neutrophils in the sputum of healthy controls ranges from 0-30% (see page 3, paragraph 3), and that asthma is associated with a percentage of sputum neutrophilia (> 90%) accompanied by a marked increase in the expression of CXCR1/2 and members of the IFN (both type I and type II interferon inducible genes) and TNF families. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 29, given that Maks et al. teach the same method of administering annexin A5 at, for example, 5 mg/kg to a subject with a lung injury , the method of Maks et al. necessarily serves the same function as the method of claim 29. In other words, if administering annexin A5 at 1mg/kg is capable of reducing pulmonary inflammatory facts, reducing pulmonary white blood cells, and/or reducing pulmonary total proteins in the instant application, it is necessarily capable of doing so in the invention of Maks et al. This is on account of the fact that "products of identical chemical composition cannot have mutually exclusive properties" (In re Spada, 911 F.2d 705, 709, 15 USPQ2d 1655, 1658 (Fed. Cir. 1990)). A chemical composition and its properties are inseparable. Therefore, if the prior art teaches the identical chemical structure, the properties applicant discloses and/or claims are necessarily present. In the case cited above, Applicant argued that the claimed composition was a pressure sensitive adhesive containing a tacky polymer while the product of the reference was hard and abrasion resistant. "The Board correctly found that the virtual identity of monomers and procedures sufficed to support a prima facie case of unpatentability of Spada’s polymer latexes for lack of novelty." In the instant case, seeing as the invention of Maks et al. uses the same chemical structure within the claimed dosage range to treat lung injury, it is inherently capable of achieving the claimed benefits of reducing inflammatory factors, reducing white blood cells, and reducing total pulmonary proteins in the lungs. Beyond this, there is no requirement that a person of ordinary skill in the art would have recognized the inherent disclosure at the relevant time, but only that the subject matter is in fact inherent in the prior art reference (Schering Corp. v. Geneva Pharm. Inc., 339 F.3d 1373, 1377, 67 USPQ2d 1664, 1668 (Fed. Cir. 2003)). See also Toro Co. v. Deere & Co., 355 F.3d 1313, 1320, 69 USPQ2d 1584, 1590 (Fed. Cir. 2004), wherein "[T]he fact that a characteristic is a necessary feature or result of a prior-art embodiment (that is itself sufficiently described and enabled) is enough for inherent anticipation, even if that fact was unknown at the time of the prior invention." Here, whether the inventors of Maks et al. explicitly teach the reduction of certain inflammatory factors or leukocytes is irrelevant to the question of whether the method is inherently capable of doing so. With regard to claim 30, as discussed above, the invention of Maks et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. As such, it is inherently capable of reducing the pulmonary inflammatory factors TNF-α, IL-10, IL-6, and/or IL-1ß. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 31, Maks et al. teach the method discussed above, but they do not explicitly teach reducing pulmonary white blood cells, neutrophils, lymphocytes, and monocytes. As discussed above, the invention of Maks et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 32, Maks et al. teach the method discussed above, but they do not explicitly teach a lowering in the quantity of pulmonary factors (E1) of an administered subject as compared to a lung injury subject (E0) at a ratio of E0/E1 is greater than or equal to 10. As discussed above, the invention of Maks et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 33, Maks et al. teach the method discussed above, but they do not explicitly teach a reduction in white blood cells of the administered subject (F1) as compared to a lung injury subject (F0) at a ratio of F0/F1 is greater than or equal to 3. As discussed above, the invention of Maks et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 34, Maks et al. teach the method discussed above, but they do not explicitly teach a reduction of total pulmonary proteins (H1) of the administered subject as compared to that of a lung injury subject at a ratio of H0/H1 is greater than or equal to 2. As discussed above, the invention of Maks et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 35, Maks et al. teach the method discussed above, but they do not explicitly teach reducing the inflammatory factors TNF-α, IL-10, IL-6, and/or IL-1ß. As discussed above, the invention of Maks et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 36, Maks et al. teach the method discussed above, but they do not explicitly teach reducing inflammatory factors in the serum of an administered subject (J1) as compared to a lung injury subject (J0) at a ratio of J0/J1 is greater than or equal to 20. As discussed above, the invention of Maks et al. comprises administering the same compound, annexin A5, and a dosage within the claimed range as compared to the instant application. Therefore, the invention of the instant application cannot have different properties, seeing as it has the same structure and dosage. Again, this represents an inherent feature in the disclosure, whether it was recognized at the time of disclosure or not. With regard to claim 38, Maks et al. teach that the pharmaceuticals of the reference application can be given in injectable form or intravenous (see [0259] ). With regard to claim 39, Maks et al. teach that the pharmaceuticals of the reference application can be administered subcutaneous ly (see [0259]). With regard to claim 40, Maks et al. teach that the pharmaceuticals of the reference application can be given in injectable , intravenous , and/or intramuscular form (see [0259]). Claim s 21-36 and 38-40 are rejected under 35 U.S.C. 102 (a)(1) and 102(a)(2) as being anticipated by US 20180015142 A1 , hereinafter Pettersson et al . , as evidenced by Laubach et al. ( Laubach, Victor E, and Irving L Kron. “Pulmonary inflammation after lung transplantation.” Surgery vol. 146,1 (2009): 1-4 ) and Zheng et al. ( Zheng, Zhikun et al. “Donor pulmonary intravascular nonclassical monocytes recruit recipient neutrophils and mediate primary lung allograft dysfunction.” Science translational medicine vol. 9,394 (2017) ) . With regard to claim 21, P e ttersson et al. teach a method of administering annexin A5 to a human patient at a dose greater than 0.1 mg/kg and up to or less than 20, 10, 5, 4, 3 or 2 mg/kg, such as about 1 mg/kg (see [0064]). Further, they teach that the annexin A5 treatment embodiments of their invention can treat lung injury (see [0026] ). With regard to claim 22, P e ttersson et al. teach that the annexin is annexin A5 (see [0064]). With regard to claim 23, P e ttersson et al. teach the method discussed above wherein the lung injury is acute lung injury (see [0095], [0096]). They also teach using annexin A5 or a function