The proposed mechanism involved a ligand–receptor interaction between TGF-β1 found in CML-derived exosomes and the TGF-β1 receptor in CML-recipient cells, causing an increase in anti-apoptotic molecules BCL-w, BCL-xl, and survivin, and reduction of the pro-apoptotic proteins BAD, BAX, and PUMA [49]. Here, BBC3 is linked to chronic myelogenous leukemia, BCR-ABL1 positive.