Indeed, individuals with EBV-associated autosomal lymphoproliferative syndrome, a primary immunodeficiency characterized by uncontrolled EBV infection, have mutations in the IL-2 inducible T cell kinase (ITK) [39–46], which is required during T cell receptor signaling as it elicits the phospholipase Cγ1 (PLCγ1)-mediated Ca2+ release upstream of the calcineurin-NFAT pathway [22]. The gene discussed is PLCG1; the disease is Epstein-Barr virus infection.