It has been suggested that inhibition of Akt signaling during the initial CAR-T cell preparation helps to maintain a T-cell memory phenotype and enhance the in vivo antitumor efficacy of CAR-T cells.67 68 However, the allosteric Akt inhibitor MK-2206, used in the study, only transiently suppresses Akt activation/phosphorylation, and phosphorylated Akt reappears in CAR-T cells before they are adoptively transferred to tumor-bearing mice; thus, the real status of Akt activation in CTLs within the TME is not addressed.68 This evidence concerns the gene AKT1 and neoplasm.