Using a mouse model for hereditary hemochromatosis, Turoczi et al. (2003) showed an interaction of dietary iron intake and HFE gene status (KO vs. wildtype) in degree of ischemia/reperfusion injury to heart; HFE KO mice showed greater ventricular dysfunction, myocardial infarct size, and cardiomyocyte apoptosis compared to wild type mice on a standard diet, and an even greater degree of damage in the HFE KO mice fed a high iron diet (Turoczi et al., 2003). This evidence concerns the gene HFE and hereditary hemochromatosis.