In particular, recent findings point to an Akt-dependent pro-tumor modulation of PKM2 72-77, which has also emerged as an upstream regulator of the PI3K/Akt pathway itself 78-81; in particular, it seems to be able to activate mTORC1 by interacting with Akt1 substrate 1 (Akt1S1) 82. This evidence concerns the gene PIK3CA and neoplasm.