This allowed assessment of the ability of EBV-specific CD8+ T cells to lyse B-LCL derived from a SAP-sufficient donor or SAP-deficient XLP patient, and thereby to determine whether the cytotoxic defect of XLP CD8+ T cells resulted from impaired presentation of EBV Ag by SAP-deficient B-LCL. This evidence concerns the gene SH2D1A and X-linked lymphoproliferative disease.