In response to infection or vaccination, CD8 T cells undergo massive proliferative expansion in numbers followed by a contraction phase where 90-95% of the expanded population is eliminated through apoptosis, with the remaining cells initiating the memory pool. Although basic CD8 T cell kinetics in response to infection and immunization have been described, the mechanisms regulating how memory CD8 T cell numbers are determined remain unknown. The current paradigm regarding memory CD8 T cell numbers states that the size of the memory pool is dictated primarily by the peak numbers achieved after infection or immunization. However, our data directly challenge this paradigm. Here, we demonstrate that DC-immunization and infection models, coupled with stimulatory IL-2/Ab complex treatment, can increase peak effector CD8 T cell numbers over 100-fold with no concurrent increase in memory CD8 T cell numbers post-contraction. Additionally, IL-2/Ab complex treatment not only increases effector CD8 T cell numbers, but also enhances and sustains expression of cytolytic molecules such as granzyme B, 4-1BB, and GITR. Thus, our data dissociate the magnitude of effector CD8 T cell expansion from memory set point, as well as highlight how IL-2/Ab complexes can enhance effector CD8 T cell function. Our findings suggest that IL-2/Ab complex therapy may be useful in short-term elevation of effector CD8 T cell numbers and function for tumor immunotherapy or during infectious disease outbreaks.