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). Here, FMO5 is linked to infection.