Furthermore, although Rottlerin has been recently reported to stimulate autophagy via inhibition of PI3K/Akt/mTOR pathway in pancreatic cancer stem cells [36], we exclude the possible negative regulation of Akt (and ERK) activity in Rottlerin-induced autophagy, since our previous study on Rottlerin-treated MCF-7 cells failed to reveal any change in the phosphorylation status of both kinases [3]. Here, AKT1 is linked to pancreatic neoplasm.