IFNA1 and COVID-19: These results are consistent with the hypothesis of a common pathogenesis for critical COVID-19 involving impaired type I IFN responses in all patients, as suggested by the similarities between patients with and without anti-IFN auto-Abs [13], and are in line with the previously suggested hypothesis of a global emerging framework of an IFN I deficiency causal for critical COVID-19, where anti-IFN auto-Abs are only one of the known and unknown mechanisms for this deficiency [22].