The excessive reactive oxygen species can activate prooncogenic signaling pathways such as receptor tyrosine kinase (RTK), phosphatidylinositol 3-kinase (PI3K)/AKT, and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), thereby aiding in cancer growth during early stages of tumorigeneses [28]. This evidence concerns the gene AKT1 and cancer.