On the other hand, high concentrations of EVE, through a massive mTORC1 inhibition, may lead to a down-regulation of S6K and a subsequent hyper-activation of mTORC2 that, sustaining the phosphorylation of AKT at S473, could induce a feedback loop that stimulates PI3K-AKT signaling activating the cellular/molecular machinery leading to renal fibrosis [45-48]. Here, AKT1 is linked to renal fibrosis.