The significant body of available data indicates that it is highly likely that the innate immune molecules SP-A1 and SP-A2 play, at the very least, an indirect role in COVID-19 infection and that in this way the SP-A variants may differentially affect disease susceptibility and/or severity or mitigate negative effects due to co-infection of COVID-19 patients with one or more non-SARS-CoV-2 pathogens [144]. The gene discussed is SFTPA2; the disease is COVID-19.