Molecular mechanisms leading to this abnormal expression include overexpression of oncogenes such as c-Myc [29], FBXO22 [30], miR-95-3p [31], deletion or mutation of tumor suppressor gene such as P53 [32], and abnormal activation of the cancer-promoting signaling pathways such as PI3K/AKT pathway [32–34]. This evidence concerns the gene AKT1 and cancer.