C5 and its cleavage product C5a are required for pulmonary accumulation of neutrophils upon infection and intravascular clearance of C. neoformans (Lovchik and Lipscomb, 1993; Sun et al., 2016), further confirming the crucial roles for C5 and C5a in neutrophil-mediated killing of C. neoformans. Jointly, these data suggest that complement activation and C5aR signaling are protective against C. neoformans-induced meningoencephalitis. The gene discussed is C5AR1; the disease is infection.