Specifically, studies evidenced, among other things, the suppression of cancer, by targeting the mTOR complex 2, as demonstrated in prostate cancer cells [317]; through the p53-dependent and p21-dependent apoptotic pathway in human hepatoma cell lines [318]; by the inhibition of AKT and ERK phosphorylation in TE1 esophageal cancer cells [319]; and by the inhibition of the ERK/MSK1 and AKT/GSK3β signaling pathways in epidermal growth factor (EGF)-induced neoplastic cell transformation by inhibiting the ERK/MSK1 and AKT/GSK3β signaling pathways [320]. The gene discussed is AKT1; the disease is prostate cancer.