We proved that senescent megakaryocytes were a major source of TGF-β1 and demonstrated that p16- and p21-double-deficient LSCs failed to increase megakaryocyte numbers at the first transplantation and lacked the leukemogenic capability to cause CML development at the secondary transplantation [164]. Here, TGFB1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.