Similarly, STAT5, a direct substrate of JAK2, is constitutively active in BCR-ABL-transduced cells [24, 25], and over-expression of Stat5 in murine BM cells generates a disease phenotype closely resembling BCR-ABL-induced CML [26]. The gene discussed is ABL1; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.