Indeed, while previous studies that examined lymphocytes from XLP patients or Sap-deficient mice have clearly shed light on the role of SAP in different immune cells and allowed us to understand the complex nature of some of the clinical manifestations of XLP [4],[7], the question of why XLP patients are uniquely susceptible to EBV infection remains unanswered. This evidence concerns the gene SH2D1A and Epstein-Barr virus infection.