Activation of SREBP-1 cleavage in tumor cells helps to maintain cell-autonomous tumor growth.4 The mTORC1 activation of S6K is thought to regulate SREBP-1 processing, giving rise to the active form that promotes transcription, including its own.5, 7 SREBP-1 cleavage and transcriptional regulation of its target FASN (fatty acid synthase) are reported to be rapamycin insensitive and AKT regulated in some tumors,19 suggesting a role for mTORC2 in the control of lipid metabolism. This evidence concerns the gene SREBF1 and neoplasm.