To account for the quite different outcomes of coronavirus disease 2019 (COVID-19), including in young people, as well as the lower prognosis of male, obese, and aged patients, we previously put forward the hypothesis that a delayed over-activation of the stimulator of interferon (IFN) genes (STING) pathway, could be central to the pathogenesis of severe COVID-19 (1, 2). The gene discussed is IFNA1; the disease is COVID-19.