A previous report showed that inhibition of BCR-ABL, as well as STAT5, by a selective inhibitor, suppressed cell proliferation and induced apoptosis in the BCR-ABL/STAT5 double positive K562 CML cell line, while this inhibitor had no effect on either a BCR-ABL-negative/STAT5-positive or a BCR-ABL/STAT5 double-negative myeloid cell line, suggesting that the STAT5 signaling pathway leading to growth and survival is BCR-ABL-dependent [44]. This evidence concerns the gene STAT5A and chronic myelogenous leukemia, BCR-ABL1 positive.