Given that there is increasing evidence of an inappropriate, inadequate type I interferon response in COVID-19 (6, 10), and that we found that sera from COVID-19 (+) patients had decreased IFNβ compared to sera from uninfected ICU patients, we postulate that this lack of IFNβ led to decreased expression of SETDB2 in Mφs, with subsequent loss of repressive H3K9me3 at NFkB-dependent inflammatory cytokine promoters, and thus an unrestricted Mφ-mediated inflammatory cytokine storm associated with coronavirus infection. This evidence concerns the gene NFKB1 and COVID-19.