AKT1 and infection: In contrast, strong and prolonged IL-2 signals may drive stronger STAT-5, Akt, mTOR and MAPK activity, thus leading to augmented proliferation, effector differentiation and migration to peripheral sites of infection, where the microenvironmental niches further reinforce the terminal differentiation programs through induction of receptors for inflammatory cytokines such as IL-12 (100), and inhibition of IL-7 (101) receptor levels.