The pathogenesis of ALI involves the activation of N-methyl-D-aspartate receptor (NMDAR) [63], simultaneously, NMDAR activation disrupts FAO by attenuating the phosphorylation and activity of PPARα through the ELK1/2 pathway, thereby promoting the lipid accumulation induced by palmitic acid [64].Overproduced ROS during ALI also results in the suppress of the expression of PPARα and CPT1A [65], while impaired FAO is also found to be associated with RIPK3-mediated necrotizing apoptosis [66]. The gene discussed is CPT1A; the disease is acute respiratory distress syndrome.