In contrast, Jia et al. (99) revealed that USP48 promoted NLRP3-dependent pyroptosis of AMs, thereby aggravating sepsis-induced ALI, whereas their subsequent work (100) identified ULK1 as a negative regulator of this process, diminishing NLRP3 expression and restraining macrophage-driven immune activation. This evidence concerns the gene NLRP3 and acute respiratory distress syndrome.