Because p53 is frequently mutated in tumors (Hollstein et al. 1999) and increased Akt kinase activity is observed in some tumor cell lines (Xu et al. 2012), more studies on 3EZ,20Ac-ingenol, which induces decatenation checkpoint through G2/M arrest by catalytic topo inhibitor and downregulates p-Akt, may provide useful information for developing anti-cancer agents. The gene discussed is AKT1; the disease is cancer.