AKT1 and neoplasm: The elevation of extracellular potassium was shown to impair T cell receptor-driven serin/threonine protein kinase B (also referred to as Akt) -mammalian target of rapamycin pathway (Akt-mTOR) phosphorylation, and thus downstream cytotoxic effector functions leading to CD8+ T cell paralysis, which was permissive for tumor growth [72].