Although the exact factors mediating distinct CD8+ T cell fates during early division following viral infection are still in the process of elucidation, experiments with TCR-transgenic mouse models indicate that TCR signaling strength (154), as reflected in IL-2R, IFN-γR, and mTOR levels during mitosis and asymmetrical division (155–157) is key to the generation of anti-viral CD8+ T cell memory. The gene discussed is CD8A; the disease is viral infectious disease.