Likewise, we observed that senescence was provoked selectively in expanding megakaryocytes in CML by an oncogenic fusion protein, BCR-ABL, and was abrogated together with megakaryocyte reduction by deletion of p16 and p21 [164], the molecules crucially involved in senescence [167]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.