In WT BMDM, both IFN-γ and IL-17A protected against infection and intracellular growth of T. cruzi. Deficiency of the gp91phox subunit of NADPH oxidase had no effect on IFN-γ-mediated protection, but reversed IL-17A-mediated protection, indicating that functional NADPH oxidase is required for this mechanism, and suggesting the involvement of ROS generated during the respiratory burst (Fig 2G). The gene discussed is IFNG; the disease is infection.