SLC39A14 and liver disorder: Using various genetic mouse models, our group and others previously showed that ferroptosis plays an important role in iron-overload-induced liver injury and fibrosis, and inhibiting ferroptosis—for example, using approaches such as Fer-1 treatment, knocking out hepatic Slc39a14, and overexpressing FGF21 (fibroblast growth factor 21) and PPARs (peroxisome proliferator-activated receptors)—has been shown to ameliorate iron-overload-induced liver disease [36,37,53,54].