SLC40A1 and Tangier disease: These observations were consistent with the findings of previous studies, where it was shown that the polymorphic variants of SLC40A1 c.44–24G>C (rs1439816) and c.663T>C (rs2304704) had a significant effect on iron metabolism and could explain the considerable unrelated HFE phenotypic variability that might exist in iron overload [9,12].