Secondly, Hh pathway could regulate autophagy in CML cells and then inhibition of the Hh pathway and autophagy simultaneously could sharply reduce cell viability and significantly induce apoptosis of imatinib-sensitive or -resistant BCR-ABL+ cells via downregulating the kinase activity of the BCR-ABL oncoprotein [165]. This evidence concerns the gene ABL1 and chronic myelogenous leukemia, BCR-ABL1 positive.