For example, SOCS1 is frequently methylated in cases of acute (AML) and chronic myeloid leukemia (CML) (123–125), which is thought to block the ability of SOCS1 to negatively regulate JAK2 activity through kinase inhibition (126), thereby promoting activation of STAT3 and STAT5 which are major drivers of leukemia development (123). This evidence concerns the gene STAT5A and chronic myelogenous leukemia, BCR-ABL1 positive.