Notably, complement activation products at the C3 level play crucial roles in controlling fungal infections, including C3b/iC3b‐mediated phagocytosis and C3a‐mediated antifungal activity.[19] Consequently, our primary focus was to analyze C3a release and C3b deposition to quantify complement activation in mice upon infection. The gene discussed is C3; the disease is fungal infectious disease.