This limited clinical penetrance may be explained in part by environmental factors,[7] including high alcohol consumption and hepatitis C virus infection for liver fibrosis or cirrhosis, but there is also evidence for genetic factors being involved.[8] For example, in a genome‐wide association studies (GWAS) in 474 unrelated p.C282Y homozygotes, single‐nucleotide polymorphism (SNP) rs3811647 in the TF gene was associated with serum iron but not clinical phenotypes.[9] It explained 7.7% of the variance of serum TF concentration and 4.7% of the variance of serum iron levels. Here, TF is linked to Hepatic fibrosis.