Herein, we have studied a subset of mTORC1-driven tumor cells using loss-of-function mutations in the Tuberous Sclerosis Complex (TSC) composed of tumor suppressor genes including TSC1 and TSC2. The proteins encoded by the TSC1 and TSC2 genes, hamartin and tuberin, respectively, interact with TBC1 domain family member 7 (TBC1D7) to form an active complex that regulates the mTORC1 activation state [8–10]. The gene discussed is TSC2; the disease is neoplasm.