Increased activation of mTORC1 is observed in numerous cancers due to alterations in intrinsic factors upstream of mTORC1 such as loss of function mutations in tumor suppressors (PTEN, Phosphatase and TENsin homolog, TP53, TSC1/2) or gain-of-function mutations in oncogenes (PI3K, Akt, Ras). Here, AKT1 is linked to cancer.