Infection with Schistosoma generally stimulates a Th1 response during the acute phase, with a consequent increase in pro-inflammatory cytokines TNFα and IFNγ, due to invasion by the larval cercaria, followed by Th1 suppression and adaptation to a Th2 response during the chronic phase of adult Schistosoma and egg release. The gene discussed is IFNG; the disease is infection.