In contrast, hematologic malignancies show divergent roles: STAT5B functions as an oncogenic driver in BCR/ABL-positive leukemia and in T-cell neoplasia harboring activating STAT5BN642H mutations, and is implicated in chronic myeloid neoplasms with eosinophilia/basophilia [15,20,21], whereas our aggregated survival analyses indicate a protective association in B-cell lymphomas. The gene discussed is ABL1; the disease is Increased total eosinophil count.