Complement (C) has emerged as a potential key contributor to the development of inflammation and tissue damage in COVID-19 patients, with the release of the pro-inflammatory peptides C3a and C5a that help to recruit leukocytes to the lung and other infected tissues and the assembly of the terminal complex that damage vascular endothelium and promotes thrombus formation [12,13]. The gene discussed is C5; the disease is COVID-19.