Kim et al. [70] reported that mTORC1 has elevated activity in most tumors due to its potential for activating oncogenes and inactivating tumor suppressors and that TGF-B may mediate glucose response through PI3K/AKT/mTOR signaling through induction by inflammatory cytokines through the expression of the HIF1A protein [71]. Here, AKT1 is linked to neoplasm.