Mills and colleagues (2016) proposed that increased mitochondrial oxidation of succinate via succinate dehydrogenase and an elevation of mitochondrial membrane potential combine to drive mitochondrial reactive oxygen species production. Thus, the same could happen in H. capsulatum, since succinate dehydrogenase was reactive to sera from patients with histoplasmosis in this study. However, H. capsulatum produces catalases that break down H2O2 into H2O and O2, working as a protection against oxidative mechanisms of the host (Maresca and Kobayashi, 2000). The gene discussed is CAT; the disease is histoplasmosis.