This result appears of peculiar relevance when considering therapeutic strategies targeting the JAK/STAT pathway in COVID-19 patients: in our hands, indeed, the inhibition of this axis effectively abrogated the synthesis of many cytokines and chemokines, but left unaffected the release of IL-8, whose crucial role in the pathogenesis of ARDS is now well recognized [53]. The gene discussed is SOAT1; the disease is acute respiratory distress syndrome.