Thus, multiple secretory effector proteins of T. gondii, including MIC1 and MIC4, appear to work in tandem to ultimately promote protective immunity by either inducing or dampening the production of proinflammatory cytokines, the timing of which is central to controlling both the parasite’s proliferation during the acute phase of infection and the induction of an effective immune response capable of establishing a chronic infection [19]. The gene discussed is CD44; the disease is infection.