Given the established role of oxidative stress in HHC development as well as the finding that an introduction of cysteine into otherwise cysteine-less K18 predisposes mice to oxidative injury [17], [18], we used previously described transgenic mice overexpressing K8 G62C to study the importance of K8 G62C in iron-overload [24]. The gene discussed is KRT18; the disease is Tangier disease.