In ARDS context, the miR-574-5p level was upregulated upon LPS stimulation via TLR/NF-κB–dependent pathways, whereas overexpression of miR-574-5p suppressed LPS-induced inflammatory responses and inhibited the activation of NF-kB signaling and the NLRP3 inflammasome through HMGB1 inhibition. The gene discussed is HMGB1; the disease is acute respiratory distress syndrome.