Activation of ERK/MAPK, JAK-STAT, ErbB, cell surface genes, genes of oxidative metabolism and DNA repair pathways, activation of inflammatory cytokines and dysregulation of key cancer signaling pathways, as well as down-regulation of pro-differentiation and TGF-β/BMP signaling pathways have also been responsible for proliferation in CML [8–10]. Here, TGFB1 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.