We have now significantly extended these observations by providing mechanistic insight into the dysfunctional behaviour of SAP− CD8+ T cells by (1) revealing that the defect in anti-EBV immunity in XLP reflects the nature of the APC, rather than EBV itself, (2) proving that NTB-A is inhibitory for the function of SAP-deficient CD8+ T cells, and (3) excluding a role for SLAM itself in regulating the function of human Ag-specific CD8+ T cells, a scenario proposed by a previous study [49]. Here, SH2D1A is linked to X-linked lymphoproliferative disease.