Our studies indicated that inhibiting the dimerization of MUC1 could significantly reduce the expression level of GPX4, decrease the expression levels of GSH and SOD, improve MDA and MPO, increase the level of lipid peroxides, break mitochondrial membrane, and increase membrane density, thereby stimulating ferroptosis and aggravating lung injury, which proved the close relationship between MUC1 and ferroptosis in the ALI model of sepsis. This evidence concerns the gene MUC1 and Sepsis.