Although studies in patients with congenital deficiency of CD154 (X-linked hyper immunoglobulin M syndrome) linked defective T cell priming and type 1 cytokine production to susceptibility to toxoplasmosis (Subauste et al., 1999), work done in CD40–/– and CD154–/– mice showed that these animals had increased susceptibility to cerebral and ocular toxoplasmosis despite seemingly unimpaired expression of IFN-γ (Reichmann et al., 2000; Portillo et al., 2010). The gene discussed is CD40; the disease is ocular toxoplasmosis.