FAH and tyrosinemia type I: Huch and colleagues16 provided the first evidence for the potential of bile duct-derived organoids as a cell therapy, first with mice and later with human-derived organoids.27 After in vitro expansion and differentiation towards the hepatocyte fate, mouse cells were successfully transplanted into a fumarylacetoacetate hydrolase (FAH)−/− mutant mice, a mouse model of hereditary tyrosinemia type I.16 Lack of FAH leads to liver failure, unless the mice are administered NTBC (2-(2-nitro-4-trifluoromethylbenzoyl)-1,3-cyclohexanedione).