PTEN (phosphatase and tensin homolog), a tumor suppressor protein, is often inactivated in cancers.21 Cellular cross-talk between PTEN and mTORC1 via the phosphatidylinositol 3 kinase (PI3K)/AKT/mTOR pathway is often deregulated and enhances the malignancy.22, 23 Although the role of mTORC1 is well characterized, the function and regulation of mTORC2 is still poorly understood. The gene discussed is AKT1; the disease is cancer.