In many myeloid and lymphoid malignancies, driver mutations resulting in constitutive JAK activation are available. The paradigm is represented by BCR-ABL1 amentoflavone substantially suppress cell proliferation, induce apoptosis and block cell cycle progression JAK2V617F can enhance the protein methylation demonstrated by activation of PRMT5 arginine methyltransferase The V617F activ... https://christophers641kpu5.wikiconversation.com/user