Findings from other cancer models suggest that NVP-BEZ235 prevents mTORC2-dependent AKTSer473 phosphorylation, and that PI3K inhibition with NVP-BEZ235 may be short-lived due to loss of feedback inhibition of PI3K activity by the mTORC1 target S6 kinase [19], [39], [69]. Here, PIK3CA is linked to cancer.