In this study, postmortem lung samples of deceased COVID-19 patients were found to have decreased expression of DOCK2 in lung lymphocytes and macrophages, and inhibition of DOCK2 in a hamster model of COVID-19 resulted in increased severity of pulmonary edema, elevated viral loads, impaired macrophage response, and dysregulated IFN responses [22]. Here, IFNA1 is linked to COVID-19.