It will be important, in future work, to explore whether the absence of systemic IFN-α, and suppressed IFNAR expression on BM LSK and circulating monocytes, as observed in our mouse model of hypoxic ALI and in hypoxemic patients with severe SARS-Cov2 infection41,42, may be sufficient to drive the phenotypic and functional changes observed in the circulating monocytes of a hypoxic ARDS cohort. The gene discussed is IFNAR1; the disease is acute respiratory distress syndrome.