Nevertheless, in ovarian cancer, abnormalities in signaling mediators, including the overexpression of epithelial growth factor receptor (EGFR) [13], self-activation of EGFR/PI3K/AKT [14,15], and PTEN dysfunction [16], result in the overactivation of signal transduction, excess production of growth and survival-related proteins, and eventually uncontrollable proliferation of anti-cancer drug tolerance in cancer cells [13,17]. This evidence concerns the gene AKT1 and cancer.