Although it has been reported in chronic hepatitis B that increased IL‐38 is associated with enhanced viral clearance upon antiviral therapy,29 high baseline IL‐38 concentrations may promote a delayed immune stimulation in the first phase of COVID‐19, thereby dampening the initial antiviral immunity and promoting over‐induction of proinflammatory mediators and severe symptoms in the late stage of the infection. The gene discussed is IL1F10; the disease is COVID-19.