These differences in progression of CML and PV suggest distinctions in the nature of BCR-ABL and JAK2 V617F oncogene-induced intrinsic and extrinsic mechanisms that govern the myeloproliferation process and its acceleration, including the rate of endogenous DNA damage, DNA damage checkpoint activation, and the extent of genomic instability. This evidence concerns the gene JAK2 and chronic myelogenous leukemia, BCR-ABL1 positive.