In contrast to highly transforming potential of BCR-ABL, the long latency of chronic indolent phase of JAK2 V617F-positive MPN (with PV being a good example), where the frequency of transformation is relatively low, supports a model in which PV progenitors avoid detrimental effects of oncogenic and oxidative stress and rather utilize signaling adaptations to extrinsic and intrinsic stresses to prevent accumulation of DNA damage. This evidence concerns the gene ABL1 and myeloproliferative neoplasm.