A third study that included seven septic patients—three of whom also developed acute respiratory distress syndrome (ARDS)—reported a clear upregulation of genes related to type I interferon signaling in ARDS, potentially driven by a virtual absence of SOCS3 (a negative regulator of cytokine signaling) in all monocyte clusters in these patients [35]. The gene discussed is SOCS3; the disease is acute respiratory distress syndrome.