Hadjadj J. et al. [80] demonstrated that in COVID-19, besides an impaired type I IFN response, severe disease correlates with an immune signature characterized by an early cytokine- and chemokine-rich inflammatory response, partially driven by NF-κB and characterized by increased TNF-α and IL-6 production and signaling, supporting a role for TLR-mediated responses. The gene discussed is NFKB1; the disease is COVID-19.