Although ectopic expression of either H1047R-PIK3CA or EGFR-L858R promoted basal Akt-T308 phosphorylation (Supplementary Fig. 10a to 10c), in response to growth stimulations including EGF (Supplementary Fig. 10d and 10e) and insulin (Supplementary Fig. 10f), hyperactivation of PI3K did not significantly promote Akt-pT308 signals in SAV1-depleted RCC cells. This evidence concerns the gene AKT1 and renal cell carcinoma.