Utilizing fumaroylacetoacetate hydrolase (FAH) mutant mice, a genetic liver disease model mimicking human type I hereditary tyrosinemia, subjected to transplantation of WT and Myc−/− hepatocytes, Edmunds et al. showed convincingly that MYC is dispensable for liver regeneration in this model (Edmunds et al., 2016). This evidence concerns the gene MYC and liver disorder.