In comparison, effector CTLs, with prolonged IL-2Rα expression, largely give rise to terminal effector and effector memory fates; and curtailed stimulation of these cells by adoptive transfer into infection-controlled recipients (removal of antigen, IL-2, and all other infection-related signals) results in less terminal differentiation, as evidenced by increased proportions of effector memory cells compared to short-lived effector cells. Here, IL2 is linked to infection.