Abstract
Hereditary hemochromatosis is the most common genetic disorder in whites. The prevalence of this condition (i.e., of homozygosity for the faulty gene) in the white population is approximately 1 in 250.1,2 The localization of the gene to the short arm of chromosome 6 (6p) by means of linkage studies confirmed the genetic nature of the disorder, but the actual gene remained elusive until the advent of positional cloning. The faulty hemochromatosis gene (HFE ) was discovered in 1996,3 and since then multiple reports have confirmed that a point mutation in HFE (the substitution of tyrosine for cysteine at . . .