Serving as the primary driver of inflammatory pathogenesis in LPS-challenged ALI, the NF-κB cascade executes its regulatory dominance through a canonical molecular sequence: IκBα phosphorylation-triggered proteolytic breakdown liberates sequestered p65 subunits for nuclear accumulation, thereby activating transcription of pro-inflammatory mediators [4]. This evidence concerns the gene NFKBIA and acute respiratory distress syndrome.