Recent studies have reported that a series of specific SMAPs reengineered from tricyclic neuroleptics effectively activate PP2A, resulting in the dephosphorylation of key targets Akt and ERK, and blocking tumor growth of lung, prostate cancer, and pancreatic neuroendocrine tumors both in vitro and in vivo [41–44]. The gene discussed is AKT1; the disease is prostate carcinoma.