SH2D1A and X-linked lymphoproliferative disease: Thus, while SAP-deficient mice have proved key to elucidating mechanisms underlying some of the immunological defects in XLP [4],[7],[9], they cannot directly address the question of EBV susceptibility because neither EBV nor its close relatives in other primates infect mice, and no mouse virus can reproduce EBV's biology or its strictly B-lymphotropic means of persistence [37].