Therefore, our findings not only provide novel insight into the roles of BPOZ as a key negative regulator of NLRP3 inflammasomes and clues to the mechanisms underlying the development of SARS-CoV-2-induced hyperinflammation, but also provide a potential therapeutic strategy for patients with SARS-CoV-2 acute respiratory distress syndrome or acute lung injury. This evidence concerns the gene NLRP3 and acute lung injury.