A recent study demonstrated widespread complement activation characterized by excessive C3a generation, C5b-9 formation, and C3d, C4d, MASP-2 deposition in lung tissues as well as prominent increase in blood C5a in proportion to the severity and high expression of C5aR in blood and pulmonary myeloid cells in patients with severe COVID-19 (56–59). This evidence concerns the gene C3 and COVID-19.