In the case of hepatic fibrosis models, the introduction of a Gpnmb transgene and Gpnmb overexpression attenuated the hepatic injury and lipid accumulation, in contrast to the adverse effects on hepatic disorder of Gpnmb gene knockout, in diet-induced [20] and carbon-tetrachloride-induced mouse models [21]. The gene discussed is GPNMB; the disease is liver disorder.