Recently, researchers demonstrated that, after pharmacological or genetic protein kinase B (AKT) inhibition, p53 interacted with sirtuin 6 (SIRT6) and poly (ADP-ribose) polymerase1 (PARP1) directly to activate it, and promoted the formation of PAR polymer in human colon cancer cell lines. This evidence concerns the gene AKT1 and colonic neoplasm.