In severe COVID‐19 cases, elevated NF‐kB activation associated with impaired IFN‐1 (Hadjadj et al, 2020) may be a host attempt to compensate for the lack of IFN‐1 activation (Rubio et al, 2013), leading to NF‐kB hyperactivation and release of pro‐inflammatory cytokines. The gene discussed is NFKB1; the disease is COVID-19.