On the other hand, studies demonstrated that the inhibitor of BCR/ABL used in the treatment against CML, imatinib, inhibits the expression of microRNA-30a in CML cells producing an increase in autophagic flux and higher levels of the proteins Beclin-1 and ATG5 [281]. This evidence concerns the gene BCR and chronic myelogenous leukemia, BCR-ABL1 positive.