Given that mTORC2 is required for oncogenic mechanism of EGFR, HER2 and loss of PTEN [43–45] and mTORC2 is also activated via genetic mutations in the mTORC2 components Rictor or Sin1 in cancer patients [46, 47], successful development of new generation mTORC1/mTORC2 inhibitors will facilitate an improved strategy for targeted cancer therapy. The gene discussed is RICTOR; the disease is cancer.