AKT1 and cancer: Conversely, pharmacological inhibition of MEK and ERK significantly increased PIK3IP1 expression in many Ras-mutant and Raf-mutant cancer cells (Fig. 5d; Supplementary Fig. 8e), while this observed de-repression of PIK3IP1 was much prominent in most of Raf-mutant cancer cells (Supplementary Fig. 8e), indicating the high MAPK activity is responsible for the suppression of PIK3IP1. Furthermore, this de-repression of PIK3IP1 correlated with concomitant inhibition of the PI3K/Akt/mTOR pathway in HCT116, A549 and transformed BJ cells, but not in those cells unable to de-repress PIK3IP1 (Fig. 5d).