Under persistent inflammatory stimulation, the NF-κB-mediated signaling pathway can upregulate the expression of key necroptotic molecules such as receptor-interacting protein kinase 1 (RIPK1) and RIPK3, activating the necroptotic program, releasing a large amount of DAMPs, leading to necroptotic and exacerbating the inflammatory response, thereby worsening the condition of ALI (146, 147). The gene discussed is RIPK1; the disease is acute respiratory distress syndrome.