The findings reported here indicate that, although the deletion of the Prdx4 gene alone had little effect on liver physiology, the deletion of Sod1 together with Prdx4 resulted in an enhanced level of aggravated liver damage compared to Sod1−/− mice (Figures 1 and 2), which reportedly develop liver steatosis [9]. Here, PRDX4 is linked to fatty liver disease.