Collectively, based on our data and the above-mentioned studies we conclude that SARS-CoV-2 infection of human monocytes, and possibly also of other myeloid cells via hijacked cyclophilins that effectively bind to myeloid-expressed CD147, contributes to hyperinflammation observed in COVID-19 patients, and that targeting the cyclophilin-CD147 axis might therefore represent another approach for alleviating the severe disease course of COVID-19. The gene discussed is PPIB; the disease is COVID-19.