This may be due to the conversion of excessive ferrous iron to hemosiderin and enhanced oxidative stress.41 Previous studies have shown that bacterial infection causes the accumulation of ferrous iron and lipid peroxidation products in RAW264.7 cells.42 We also noted this in both RAW264.7 and Gsta4-deficient 2D6 cells after E. faecalis infection. This evidence concerns the gene GSTA4 and bacterial infectious disease.