Although mTORC1 activation is known to suppress autophagy through phosphorylation of ULK1 at Ser75751,52, recent studies also suggested that selective autophagy such as lipophagy could play a role for sustaining mTORC1 activation and fulfilling increased bioenergetic demands in Tsc-deficient neural stem cells, as well as some tumor cells under energy stressed conditions35,38. This evidence concerns the gene TSC1 and neoplasm.