It is worth pointing out that the link between AKT activation and O2.−-mediated Mcl-1 accumulation is not exclusive to hematopoietic cancers; stable knockout of AKT1/2 in HCT116 colorectal carcinoma cells (AKT-DKO) also exhibited reduced T163pMcl-1 and Mcl-1 levels, which was not due to reduction in MCL1 mRNA levels (Fig. S10B, C). This evidence concerns the gene AKT1 and hematopoietic and lymphoid cell neoplasm.