Investigating the underlying mechanism of action, Zeng et al. observed that combined inhibition (Hh and autophagy) in CML cells led to downregulation of the kinase activity of BCR-ABL oncoprotein and components of the PI3K/Akt/mTOR pathway, suggesting that Hh inhibition induced cytoprotective autophagy and downregulated the Pi3k/Akt pathway [114]. The gene discussed is PIK3CD; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.