It can bind with K-Ras [32] to activate downstream signalling pathways, including PI3K/Akt, PLC/PKC, Raf/MEK/ERK, RALGDS/Ral, and TIAM1/Rac, to promote cancer cell survival, migration, invasion, and cell cycle progression through the hijacking of the upstream receptor tyrosine kinases, such as epidermal growth factor receptor (EGFR) and insulin-like growth factor receptors (IGFRs), as well as G-protein coupling receptors (GPCRs) [33]. This evidence concerns the gene AKT1 and cancer.