These results suggest that while the carriage of IFNAR2 p.F8S predisposes to severe COVID-19 leading to hospitalization, the mechanism does not seem to be related to increased vulnerability to progressive lung damage, coagulopathy, nor to impaired control of viral replication, but it may encompass a pro-inflammatory effect linked to upregulation of IL-6 secretion. Here, IL6 is linked to COVID-19.