In septic ALI, heat shock factor 1 (HSF1) inhibited the NF-κB signaling pathway by upregulating tumor necrosis factor receptor-associated factors 3(TRAF3)expression, thereby inhibiting the production of NLRP3 at the transcriptional level and ultimately inhibiting the activation of the NLRP3 inflammasome, which reduces macrophage pyroptosis and subsequently alleviates pulmonary damage (122). This evidence concerns the gene NLRP3 and acute respiratory distress syndrome.