Several studies have reported that ApoA-I and HDL-C are less abundant in COVID-19 patients (Poynard et al., 2020; Sun et al., 2020; Begue et al., 2021; Hilser et al., 2021), especially in the most severe forms, and that HDL-C from COVID-19 patients is less protective in endothelial cells submitted to inflammatory triggers and does not protect them from apoptosis (Begue et al., 2021). The gene discussed is APOA1; the disease is COVID-19.