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). The gene discussed is JAK2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.