We therefore hypothesised that the temporal dysregulation in the magnitude (and quality) of the Th1 response in malaria-infected WSX-1−/− mice was a direct consequence of the reinforcement of Th1 molecular programming in WSX-1−/− mice, potentiating T-bet expression and terminal differentiation of effector CD4+T-bet+ T cells. The gene discussed is CD4; the disease is malaria.