AKT (serine/threonine kinase or protein kinase B, PKB) is recognized to be a major oncogenic regulator of this pathway, and its consistent overexpression/activation observed in tumor cells is related to blocking of drug-induced apoptosis via multiple mechanisms, such as amplifying the effect of anti-apoptotic modulators (Bcl-2 and survivin) and counteracting the functions of pro-apoptotic (Bax, Bad, and p53) proteins [54,55]. This evidence concerns the gene BCL2 and neoplasm.