PI3K/mTORC1 is frequently activated in human cancers by gain-of-function mutations and amplifications of its upstream activators - such as epidermal growth factor receptor (EGFR), HER2 [13], PI3K or protein kinase B (AKT) - and by the loss of its suppressors, such as phosphatase and tensin homologue (PTEN) [14], inositol polyphosphate-4-phosphatase, type II (INPP4B) [15], or the tuberous sclerosis complex (TSC), mediated by the tumor suppressor genes, TSC1 and TSC2[16,17]. This evidence concerns the gene AKT1 and cancer.