Furthermore, bacterial products such as 16S rRNA and LPS have been detected in severe/critical COVID-19 patients even in the absence of bacterial infections [42] and it is known that patients with severe COVID-19 have decreased IgG fucosylation and increased levels of IgG3, IgM, and IgA [43], which promotes spontaneous release of NETs through the activation of the FcγR [10]. This evidence concerns the gene CD79A and bacterial infectious disease.