While each piece of clinical evidence discussed does not by itself provide overwhelming corroboration for the hypothesis of the paper, the totality of evidence presented we believe make a strong case that if sequence and/or structural mimicry to hepcidin is taking place upon viral attachment to and entry in the host cell, then perhaps a local disease condition resembling iron dysregulation (e.g., iron overload) might ensue in the infected tissue(s). The gene discussed is HAMP; the disease is Tangier disease.