Clinical data have demonstrated evidence of increased C3a and C5a complement production, “cytokine storm,” proinflammatory macrophage accumulation, and cellular apoptosis in COVID-19 and other lung diseases (20, 49). Previous work in our laboratory demonstrated that activation of the complement cascade was consistently observed in a perivascular-specific manner in human PAH and laboratory animal models of hypoxic pulmonary hypertension (27). The gene discussed is C3; the disease is lung disorder.