Defective signaling lymphocyte activation molecule (SLAM)‐associated protein (SAP) is responsible for the human X‐linked lymphoproliferative syndrome. Defects in T helper 2, natural killer, natural killer T and B cells have been demonstrated in SAP‐deficient humans and mice, and increased proliferation of CD8⁺ T cells has been observed. In the current study, we investigated the properties of CD8⁺ T cell proliferation and activation‐induced cell death (AICD), using OT‐I T cell receptor (TCR)‐transgenic mice on either wild‐type (WT) or SAP^–/– background. Interestingly, we found that ovalbumin peptide‐activated SAP^–/– CD8⁺ T cells have lower AICD compared to their WT counterparts. Furthermore, the induction of p73, a key mediator of TCR‐induced apoptosis through the mitochondrial apoptotic pathway, was significantly reduced at both the mRNA and protein levels in the activated mutant cells. Meanwhile, a reduced level of activated caspase 9 was observed in the mutant cells. We conclude that reduced AICD in activated SAP^–/– CD8⁺ T cells is associated with impaired p73 induction, indicating that the initiation of the mitochondrial apoptotic pathway might be impaired. Our data demonstrate an intrinsic defect in SAP^–/– CD8⁺ T cells and shed light on the increased responsiveness of CD8⁺ T cells in SAP^–/– mice.