Abstract One important feature of T-cell memory formation is the process of cell death during the contraction phase of the immune response. CD8 T-cell contraction after acute infections is mediated by the intrinsic apoptosis pathway, regulated by the interaction of anti-apoptotic BCL2 with pro-apoptotic Bim. In a murine model of influenza A virus infection, we found that Bim-deficient animals experienced a total ablation of the CD8+ T cell contraction phase leading to the significant accumulation of antigen-specific cells. While these cells displayed typical memory phenotypes, in vivo adoptive transfer and in vitro functional studies show that Bim-deficient memory CD8 T cells are non-responsive to stimulation by antigenic peptides and fail to expand properly on secondary challenge, indicating an intrinsic defect of this spent effector population. These functional deficiencies begin to emerge even at the peak of the primary response. Taken together, these results demonstrate that efficient memory generation entails the generation of a distinct, productive memory lineage that is capable of evading Bim-mediated apoptosis.