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The hereditary haemochromatosis gene (HFE) has recently been proposed as a disease modifying gene.1 The rationale is that two common mutations of the HFE gene (C282Y and H63D) are found in a majority of patients with genetic haemochromatosis who are either homozygotes (C282Y/C282Y) or compound heterozygotes (C282Y/H63D). These mutations have been shown to contribute to more subtle modifications of iron homeostasis at the heterozygous state.2 In turn, iron may predispose to myocardial damage through the production of activated oxygen species. Recently, Mahon and colleagues have reported an association between the H63D mutation and idiopathic dilated cardiomyopathy (IDCM).3 In this study, 207 unrelated white patients with dilated cardiomyopathy and 200 controls were tested for HFE C282Y and H63D mutations. An increased proportion of H63D heterozygotes was found among patients (36%) as compared to the control group (27%). No association was found with C282Y mutation and as the H63D mutation had a relatively minor effect on iron status, these authors proposed that this association may be …