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. DETAILED ACTION Claims 21-29 are pending. Claims 21-29 are under examination on the merits. Priority Applicant’s claim for the benefit of a prior-filed application under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged. Claims 21-29 have an effective filing date o f 06/30/2017, corresponding to PRO 62/527,798. Information Disclosure Statement The information disclosure statemen t (IDS) submitted o n 02/29/2024 is in compliance with the provisions of 37 CFR 1.97. Accordingly the information disclosure statement is being considered by the examiner. Notes on the Prior Art The prior art does not teach or suggest a method of reducing leukemia relapse in a subject in need thereof (or a method to inhibit or reverse hematological cancer cell colonization of the central nervous system (CNS) in a subject in need thereof ) , the method comprising administering to the subject, a Protocadherin-9 (PCDH9) inhibitor, wherein the PCDH9 inhibitor is selected from the group consisting of an antisense molecule, an siRNA molecule, an shRNA molecule, a B-cell directed antibody and a nanoparticle loaded with PCDH9-specific interfering RNA. At the effective filing date of the invention, it was known in the art that PCDH9 is expressed on ca nc er cells. For example Maheswaran et al. (WO 2013/049680, international publication date: 04/04/2013) teach that PCDH9 is a tumor marker - “I n an additional aspect, the invention features methods for diagnosing cancer in a subject. The methods include providing a sample comprising blood from the subject; contacting the sample with one or more agents that bind to a cancer cell surface marker selected from the group consisting of cadherin 1 ( CDHl ), CDH2, CDH3, CDH4, CDH5, CDH9, CDHl 1, CDHl 7, CDHl 9, protocadherin 9 (PCDH9) and/or PCDH beta 13 ( PCDHb 13), under conditions sufficient to allow binding of the agent to cells expressing the surface marker; and detecting the binding of the agent to a cancer cell surface marker present on a cell in the sample; wherein the presence of binding to a cell in the sample indicates that the subject has cancer (emphasis added).” See p.2. At [0031], Rosner et al . (US PG PUB 20160078167, publication date: 03-17-2016) teach that PCDH9 activity or expression may be used to determine whether a breast cancer patient is likely to respond to DNMT inhibitor therapy - “ In some embodiments, the method comprises or further comprises measuring the level of expression or activity in the breast cancer sample of TET1 and comparing the level of expression or activity of TET1 to a referce expression level or activity. In some embodiments, a patient's response to DNMT inhibitor therapy is predicted based on the compared expression level or activity. In some embodiments, the method includes measuring the activity of TET1. In some embodiments, measuring the activity of TET1 comprises measuring the level of expression of any of TET1 target genes, including, but not limited to, one, two, or more of AKAP12, APOC1, BAI3, BRWD1, CA2, CALCRL, CAMKV, CDC37L1, CNTN1, COX7C, DIXDC1, DLX2, DSC2, DYNC2LI1, EML1, EPHA3, EPHA7, EPHB1, EPM2AIP1, ERC2, FABP6, FLRT3, GFOD2, GPM6B, H3F3A, HEY1, HIST1H2BJ, HMGN3, HNRNPA1, HOXD13, IFT57, IFT81, JHDM1D, KCNJ2, KLHL3, LMBR1L, LOC646934, LPHN2, LPHN3, LRP1B, LZTFL1, MOAP1, NDUFA1, NDUFB4, NEBL, NEK3, NR2F1, NUP62CL, PAK1, PCDH17, PCDH7, PCDH9 , PDE5A, PES1, PLTP, PTPRB, RAB40A, RAPGEF4, RARB, RBM3, RNF128, RPL3, RPL35, RPL36A, RPL39, SEPP1, SERPINF1, SLC13A4, SNCA, SPON1, SPPL2B, STK38L, SYT1, TCF4, TGDS, TSC22D3, TSPAN7, UXT, VAV1, WDR48, ZNF74 and ZNF84. In some embodiments, a patient is predicted to respond to DNMT inhibitor therapy when the expression or activity of TET1 is lower than the reference level (emphasis added) . ” Although it was known in the art at the effective filing date of the claimed invention that PCDH9 is expressed on cancer cells, the prior art does not teach or suggest a method of reducing leukemia relapse in a subject in need thereof (or a method to inhibit or reverse hematological cancer cell colonization of the central nervous system (CNS) in a subject in need thereof ) , the method comprising administering to the subject, a Protocadherin-9 (PCDH9) inhibitor , as instantly claimed. Furthermore following a review of the prior art, it was determined that the prior art does not teach or suggest methods of treating cancer via the administration of a PCDH9 inhibitor. For example Parsons et al. (US PG PUB 2008/0095764, publication date: 04/24/2008 , IDS ) discuss the functions of various protocadherins in cancer, and the teachings of Parsons et al. would have provided no motivation for one of ordinary skill in the art to develop the instantly claimed invention. At [0013], [0014], and [0016], Parsons et al. teach that “[t]he present invention is based upon the surprising discovery that human protocadherins on chromosome 13q 14-21 are activated or inactivated, as the case may be, in an oncogenic switch. For example, the inventors have discovered that protocadherin 17 is turned on, and protocadherins 8 and 9 are shut off, in cancer… Accordingly, in one aspect, the present invention provides a method for determining whether a subject has neoplasia, by assaying a diagnostic sample of the subject for expression of at least one protocadherin selected from the group consisting of PCDH8, PCDH9, and PCDH17, wherein detection of PCDH8 expression decreased below normal is diagnostic of neoplasia in the subject, detection of PCDH9 expression decreased below normal is diagnostic of neoplasia in the subject, and detection of PCDH17 expression elevated above normal is diagnostic of neoplasia in the subject… The present invention also provides a method for assessing the prognosis of a subject who has neoplasia, by assaying a diagnostic sample of the subject for expression of at least one protocadherin selected from the group consisting of PCDH8, PCDH9, and PCDH17, wherein the subject’ s prognosis improves with an increase in expression of PCDH8 in the diagnostic sample and/or an increase in expression of PCDH9 in the diagnostic sample and/or a decrease in expression of PCDH17 in the diagnostic sample, and wherein the subject ’ s prognosis worsens with a decrease in expression of PCDH8 in the diagnostic sample and/or a decrease in expression of PCDH9 in the diagnostic sample and/or an increase in expression of PCDH17 in the diagnostic sample. ” At [0024] Parsons et al. teach that “ the present invention provides a method for identifying an agent for use in treating and/or preventing neoplasia, by: (a) obtaining a collection of cells having at least one characteristic selected from the group consisting of PCDH8 expression decreased below normal, PCDH9 expression decreased below normal, and PCDH17 expression elevated above normal; (b) contacting a candidate agent with the cells; and (c) determining the effect, if any, of the candidate agent on PCDH8 expression, PCDH9 expression, and/or PCDH17 expression in the cells. ” Also at [0046] Parsons et al. teach that “ the inventors have discovered that human protocadherins on chromosome 13q14-21 are activated or inactivated, as the case may be, in an oncogenic switch. For example, the inventors have discovered that protocadherin 17 is turned on, and protocadherins 8 and 9 are shut off, in cancer. In normal breast cells, protocadherin 17 is typically silent, while protocadherins 8 and 9 are typically expressed. Contrastingly, in breast cancer, protocadherin 17 is expressed, while protocadherins 8 and 9 are either mutated or silenced through methylation of their promoters. Altered expression of these genes is also seen in prostate cancer. ” Therefore Parsons et al. teach or suggest that it is the absence or downregulation of PCDH9 that is associated with cancer, and Parsons et al. teach that a subject’s prognosis worsens with a decrease in the expression of PCDH9 i n a diagnostic sample . These teachings are effectively the opposite of what is instantly claimed and disclosed. For example, as indicated above, at p. 6 of the specification, it is disclosed that “P CDH9 is a transmembrane adhesion receptor of the protocadherin family, which is known to mediate calcium-dependent cell adhesion in neuronal tissues ( Strehl , S., Glatt, K., Liu, Q.M., Glatt, H. & Lalande , M. Characterization of two novel protocadherins (PCDH8 and PCDH9) localized on human chromosome 13 and mouse chromosome 14. Genomics 53 , 81-89 (1998)). PCDH9 was virtually absent in the B-ALL line that exhibited a systemic phenotype, and was highly expressed (>27-fold) in the B-ALL line with the CNS colonization phenotype by both mRNA and Western Blot analysis (Table 1, Fig. 2). PCDH9 is not expressed in normal leukocytes, but gene profiling of leukemia patient samples available in public databases shows that PCDH9 is ectopically expressed in various human leukemia samples. PCDH9 upregulation is also a poor prognostic factor in ALL (Silveira, V.S. et al . Gene expression pattern contributing to prognostic factors in childhood acute lymphoblastic leukemia. Leukemia & lymphoma 54, 310 -314 (2013)). PCDH9 depletion in leukemia cells greatly reduces their ability to give rise to CNS pathology (Fig. 4). Based on these data, ectopic expression of PCDH9 in leukemia cells is expected to enable leukemia cells to colonize the CNS and cause CNS pathology and relapses. Both the mouse ALL model just described and a human ALL xenograft model that also gives rise to CNS pathology in recipient mice can be used (emphasis added) . ” 35 U.S.C. 112(a) 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. Claims 21-29 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for pre-AIA the inventor(s), at the time the application was filed, had possession of the claimed invention. A determination of whether a claimed invention is compliant with the written description requirement of 35 U.S.C. 112, is made based on the considerations that are outlined in Guidelines for Examination of Patent Applications Under the 35 U.S.C. 112, ¶ 1 “Written Description” Requirement , Federal Register, Vol. 66, No. 4, 01/05/2001, hereinafter referred to as “Guidelines”. The “Guidelines” state that when a patent application is filed, there is a strong presumption that adequate written description under 35 U.S.C. 112, first paragraph, is present, however: “The issue of a lack of adequate written description may arise even for an original claimed when an aspect of the claimed invention has not been described with sufficient particularity such that one skilled in the art would recognize that the applicant had possession of the claimed invention. The claimed invention as a whole may not be adequately described if the claims require an essential or critical feature which is not adequately described in the specification and which is not conventional in the art or known to one of ordinary skill in the art. This problem may arise where an invention is described solely in terms of a method of its making coupled with its function and there is no described or art-recognized correlation or relationship between the structure of the invention and its function. A lack of adequate written description issue also arises if the knowledge and level of skill in the art would not permit one skilled in the art to immediately envisage the product claimed from the disclosed process.” See p. 1105, first column. Furthermore, in Vas-Cath v. Mahurkar , 935 F.2d 1555 (1991), the Federal Circuit, in quoting In re Driscoll , 562 F.2d 1245, 1250, 195 USPQ 434, 438 (CCPA 1997), stated that “[I]t should be readily apparent from recent decisions of this court involving the question of compliance with the written description requirement of § 112 that each case must be decided on its own facts. Thus, the precedential value of cases in this area is extremely limited.” Id . at 1562. Additionally, the Federal Circuit has explained that claim language, even original claim language, having ipsis verbis (i.e., in the same words) support in the specification does not necessarily establish compliance with the written description requirement. As stated in Enzo Biochem , Inc. v. Gen-Probe Incorporated , 323 F.3d 956 (2002): “Even if a claim is supported by the specification, the language of the specification, to the extent possible, must describe the claimed invention so that one skilled in the art can recognize what is claimed. The appearance of mere indistinct words in a specification or a claim, even an original claim, does not necessarily satisfy that requirement. One may consider examples from the chemical arts. A description of an anti-inflammatory steroid, i.e., a steroid (a generic structural term) described even in terms of its function of lessening inflammation of tissues fails to distinguish any steroid from others having the same activity or function. Similarly, the expression [“]an antibiotic penicillin[”] fails to distinguish a particular penicillin molecule from others possessing the same activity. A description of what a material does, rather than of what it is, usually does not suffice. (emphasis added)” Id. At 968. Thus, even original claims that are fully supported by the specification must comply with the written description requirement, which establishes that the inventor was in possession of the claimed invention at the time of filing. The claims are drawn to various genera of PCDH9 inhibitors, such as antisense molecules, siRNA molecules, shRNA molecules, a B-cell directed antibody, and a nanoparticle loaded with PCDH9-specific interfering RNA. Throughout the specification, Applicant discusses antisense molecules, such as PCDH9 shRNA (PCDH9 KD), as PCDH9 inhibitors, and one skilled in the art can readily envision inhibitors of PCDH9 that are antisense molecules, siRNA molecules, or shRNA molecules. However absent empirical determination, one skilled in the art would be unable to readily envision at least most of the antibodies that are encompassed in the genus of PCDH9 inhibitors . For example in the absence of empirical determination, one skilled in the art would not be able to determine whether a particular antibody is capable of inhibiting PCDH9. The written description requirement for a claimed genus may be satisfied through sufficient description of a representative number of species by actual reduction to practice, reduction to drawings, or by disclosure of relevant, identifying characteristics, i.e., structure or other physical and/or chemical properties, by functional characteristics coupled with a known or disclosed correlation between function and structure, or by a combination of such identifying characteristics, sufficient to show that Applicant was in possession of the claimed genus. See Eli Lilly , 119 F.3d at 1568, 43 USPQ2d at 1406. A “representative number of species” means that the species which are adequately described are representative of the entire genus. Thus when there is substantial variation within the genus, one must describe a sufficient variety of species to reflect the variation within the genus. The broad range of species encompassed by the claimed genera of PCDH9 inhibitors that are antibodies is highly variant, and Applicant does not appear to have disclosed any antibodies that are capable of targeting and inhibiting the function of PCDH9. Furthermore Applicant has not provided any general structure of anti-PCDH9 antibodies that correlates with the claimed functional ability of inhibiting PCDH9. The ability of an antibody to bind a particular antigen, such as PCDH9, does not characterize what other properties the antibody may or may not possess. It is well-recognized in the art that antibodies will display markedly different and unpredictable properties depending on the epitope in an antigen to which the antibody specifically binds. Stancovski et al. (PNAS, 88: 8691-8695, 1991 , IDS ) developed a panel of monoclonal antibodies specific to HER-2, an art-known tumor antigen, and Stancovski et al. discovered that although each antibody bound the HER-2 antigen, said antibodies displayed a range of different properties, see Abstract and p. 8694, Table 1. Two of the anti-HER-2 antibodies almost completely inhibited tumor growth, two anti-HER-2 antibodies displayed moderate inhibitory effects, and yet another anti-HER-2 antibody accelerated tumor growth, p. 8694, Table 1. Additionally, said panel of anti-HER-2 antibodies demonstrated a range of apparent affinities and a range of abilities to induce complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and tyrosine phosphorylation, p. 8694, Table 1, and p. 8692, second column, second full paragraph. Furthermore, similar to Stancovski et al., Jiang et al. (J. Biol. Chem., 280: 4656-4662, 2005 , IDS ) teach that while many anti-HER-2 antibodies inhibit the proliferation of cancer cells, other anti-HER-2 antibodies actively stimulate cancer growth, see p. 4656, second column, final paragraph. Importantly, Jiang et al. add that “[ i ]t is well known that different biological effects are associated with the epitope specificity of the antibodies.” See p. 4656, second column, final paragraph. Based upon the teachings of Stancovski et al. and Jiang et al., one skilled in the art would appreciate that antibodies specific for the same target protein may have different effects depending upon the epitope specificity of a particular target protein-specific antibody. One skilled in the art would reason that the PCDH9 protein comprises numerous B cell epitopes. Some of said B cell epitopes would be expected to serve as targets for anti-PCDH9 antibodies that inhibit PCDH9 function, while other B cell epitopes would be expected to serve as targets for anti-PCDH9 antibodies that either do not inhibit PCDH9 function, or potentially promote PCDH9 function. Therefore it is submitted that in the absence of empirical determination, one skilled in the art would be unable to readily envision the structure of a particular anti-PCDH9 antibody that is capable of binding to PCD H 9 and inhibiting PCDH9 function. Although screening techniques can be used to isolate antibodies that are capable of inhibiting PCDH9 function, Applicant is reminded that the written description requirement of 35 U.S.C. 112 is severable from the enablement provision. As stated in Vas-Cath Inc. v. Mahurkar (CA FC) 19 USPQ2d 1111, 935 F2d 1555, “The purpose of the ‘written description’ requirement is broader than to merely explain how to ‘make and use’; the applicant must also convey with reasonable clarity to those skilled in the art that, as of the filing date sought, he or she was in possession of the invention. The invention is, for purposes of the ‘written description’ inquiry, whatever is now claimed.” It is further noted that the method of claim 25 encompasses a large genus of hematological cancers. At p. 6-8 of the specification, it is disclosed that “PCDH9 is a transmembrane adhesion receptor of the protocadherin family, which is known to mediate calcium-dependent cell adhesion in neuronal tissues ( Strehl , S., Glatt, K., Liu, Q.M., Glatt, H. & Lalande , M. Characterization of two novel protocadherins (PCDH8 and PCDH9) localized on human chromosome 13 and mouse chromosome 14. Genomics 53, 81-89 (1998)). PCDH9 was virtually absent in the B-ALL line that exhibited a systemic phenotype, and was highly expressed (>27-fold) in the B-ALL line with the CNS colonization phenotype by both mRNA and Western Blot analysis (Table 1, Fig. 2). PCDH9 is not expressed in normal leukocytes, but gene profiling of leukemia patient samples available in public databases shows that PCDH9 is ectopically expressed in various human leukemia samples. PCDH9 upregulation is also a poor prognostic factor in ALL (Silveira, V.S. et al. Gene expression pattern contributing to prognostic factors in childhood acute lymphoblastic leukemia. Leukemia & lymphoma 54, 310-314 (2013)). PCDH9 depletion in leukemia cells greatly reduces their ability to give rise to CNS pathology (Fig. 4). Based on these data, ectopic expression of PCDH9 in leukemia cells is expected to enable leukemia cells to colonize the CNS and cause CNS pathology and relapses. Both the mouse ALL model just described and a human ALL xenograft model that also gives rise to CNS pathology in recipient mice can be used (emphasis added).” At p. 7 of the specification, it is disclosed that “[ i ]dentification of PCDH9 as a novel target for prevention of leukemia CNS relapses: Relatively little is known about PCDH9. It belongs to the protocadherin family, a group of transmembrane proteins that mediate Ca 2+ -dependent homotypic cell adhesion. PCDH9 is predominantly expressed in neuronal tissues and not normally expressed in leukocytes ( Strehl , S., Glatt, K., Liu, Q.M., Glatt, H. & Lalande , M. Characterization of two novel protocadherins (PCDH8 and PCDH9) localized on human chromosome 13 and mouse chromosome 14. Genomics 53 , 81-89 (1998)). Ectopic expression of PCDH9 in human leukemia cells has been demonstrated by expression profiling, and includes but is not limited to human ALL. Furthermore, PCDH9 expression is a poor prognostic factor in ALL (Silveira, V.S. et al. Gene expression pattern contributing to prognostic factors in childhood acute lymphoblastic leukemia. Leukemia & lymphoma 54, 310-314 (2013)). Ectopic expression of PCDH9 in leukemia cells is believed to allow them to adhere and interact with neuronal and/or glial cells enabling the leukemia cells to establish a niche in the CNS… Use of PCDH9 as a new diagnostic tool to predict the risk of CNS colonization: PCDH9 expression in leukemia cells is a factor that enables leukemia cells to colonize the CNS which allows for staining leukemia cells from a patient’s blood sample for PCDH9 expression. This is a novel and greatly improved method to establish the risk for CNS colonization in leukemia patients. This enables more effective treatment stratification, thereby reducing the need and intensity of harmful CNS-directed therapies in lower risk patients.” Based upon this passage, one of ordinary skill in the art would reason that the expression of PCDH9 in leukemia or lymphoma cells represents a poor prognosis for a leukemia or lymphoma patient, in part, because the expression of PCDH9 in leukemia or lymphoma cells may allow for CNS colonization. One of ordinary skill in the art would also appreciate that administering a PCDH9 inhibitor to a leukemia or lymphoma patient having PCDH9-expressing cancer cells may represent a means of treating said patient ; h owever Applicant has not demonstrated PCDH9 expression in any other types of hematological cancers. To conclude given 1) the lack of particularity with which the claimed PCDH9 inhibitors are described in the specification and 2) the breath of treatable cancers claimed, it is the Examiner’s position that in the absence of empirical determination, one skilled in the art would be unable to practice the instantly claimed invention. Furthermore the instant disclosure does not sufficiently demonstrate that Applicant was in possession of the claimed invention at the time of filing. The claims therefore fail to satisfy the written description requirement of 35 U.S.C. 112, first paragraph. Nonstatutory Double Patenting The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg , 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman , 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi , 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum , 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel , 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington , 418 F.2d 528, 163 USPQ 644 (CCPA 1969). A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA. A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b). The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13. The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA/25, or PTO/AIA/26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer . Claims 21-29 rejected on the ground of nonstatutory double patenting a s being unpatentable over claims 1-4 of U.S. Patent No. 11,002,740 . Although the claims at issue are not identical, they are not patentably distinct from each other , because both sets of claims encompass the treatment of leukemia or lymphoma comprising administering to a subject in need thereof a PCDH9 inhibitor, wherein said PCDH9 inhibitor is selected from the group consisting of an antisense molecule, an siRNA molecule, and an shRNA molecule , wherein the leukemia is Acute Lymphoblastic Leukemia (ALL) or Acute Myeloid Leukemia (AML) , and wherein the subject is human. Conclusion No claims are allowed. 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