SLC39A14 and Hepatic fibrosis: It has been shown that the knockout of TRF in hepatocytes from mice resulted in the accumulation of non-transferrin bound iron in the liver, which further aggravated liver fibrosis mediated by a high iron diet, while the specific knockout of TRF and solute carrier family 39 member 14 (SLC39A14) could significantly reduce the accumulation of iron in the liver, leading to improved liver fibrosis mediated by a high iron diet or carbon tetrachloride injection (Jenkitkasemwong et al., 2015).