Moreover, bone marrow-derived cells, and in particular macrophages, have been shown to suppress the lethality of mice lacking the fumaryl acetoacetate hydrolase gene Fah, a preclinical model of hereditary tyrosinemia type I; this occurs via fusion of donor cells with Fah-deficient hepatocytes, thereby restoring hepatocyte viability and function [55]. This evidence concerns the gene FAH and tyrosinemia type I.