High levels of AKT can inhibit homologous recombination (HR) repair by suppressing the formation of BRCA1 and Rad51 foci, specifically after exposure to Irradiation (IR) in breast cancer.25 Overactivated AKT or PTEN loss can also overcome the DNA damage-induced G2 cell cycle checkpoint and Chk1 activation upon exposure to genotoxic stresses.23, 26, 27, 28, 29 Thus, neoplastic cells expressing constitutively active AKT can avoid apoptosis and checkpoint-dependent cell cycle arrest, and accumulate potential cancer-causing mutations due to suppression of HR and reliance on error-prone NHEJ. This evidence concerns the gene AKT1 and cancer.