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Abstract Introduction: Philadelphia chromosome-like acute lymphoblastic leukemia (Ph-like ALL) is a neoplastic proliferation of lymphoblasts that has a gene expression profile similar to that of BCR-ABL1 positive B-ALL, but lacks the disease-defining Philadelphia chromosome. Growing evidence has proved that alterations in the cytokine receptor-like factor 2 gene (CRLF2)that result in CRLF2 overexpression associates with poor treatment outcomes thus highlighting a potentially important oncogenic mechanism in a subset of patients. The significant association of CRLF2 overexpression with JAK2 mutation suggests that these patients may benefit from future kinase inhibitor approaches. In addition, cell surface-expressed CRLF2 itself may be a potential target for anti-CRLF2 antibody based therapies |