ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive: 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.