In addition to the PIK3CA mutant tumor cells as we tested in this study, we and others also observed that in KRAS mutant and wild-type colon and lung cancer cells, rapamycin could also elicit AKT activation and increase the level of AKT-mediated phosphorylation of PRAS40 on Thr246 (Supplementary Figure 5) [38]. This evidence concerns the gene AKT1 and neoplasm.