This PR/CR rate is lower than the rate we previously reported for gynecologic and breast malignancies, in which the PR/CR rate was 30%, and may be due to the fact that the largest subgroup (colorectal cancer) in this paper did not respond well to PI3K/AKT/mTOR axis therapy even in the presence of PIK3CA mutations.[16] The lack of response may be due to the high rate of concomitant MAPK mutations in colorectal cancer. Here, AKT1 is linked to colorectal cancer.