FAH and steatosis: While this comparison is not ideal given the predisposing Trp53 mutation in one group and not the other, investigators chose to pursue in vivo analyses of two candidate genes enriched in tumors from the steatosis cohort, Prkaca and Nat10. Vectors expressing either constitutively active Prkaca (PrkacaL206R), fumarylacetoacetate hydrolase (Fah), and short hairpin RNA targeting Trp53 (shTrp53) or Fah and shTrp53 alone were introduced into Fah-deficient male and female mice on either the steatosis-inducing treatment diet or normal diet.