Resistance to the parasite Toxoplasma gondii is characterized by an acute phase of infection associated with activation of innate immune cells such as neutrophils, dendritic cells (DCs), and macrophages that produce IL-12, which promotes NK and T cell production of IFN-γ [1], [2] These events lead to the early control of parasite replication and the transition into the chronic phase of infection where the parasite persists as tissue cysts, most notably within the CNS [3]–[5]. The gene discussed is IFNG; the disease is infection.