In vivo phosphorylation levels of Akt, mTOR and FoxO1/O3, a critical regulator of T cell homeostasis activated by PI3K/Akt pathway, showed dynamic alterations during the course of infection: while Akt activation correlated with mTOR activity, no correlation was observed in FoxO1/O3 phosphorylation, inhibiting thus apoptosis of infected lymphocytes [89]. The gene discussed is AKT1; the disease is infection.