These results are consistent with human genetics where carriers of MTARC1 loss of function variants are protected from all-cause cirrhosis12 but contrasts with recent findings by Smagris et al31 who observed no effect of the genetic deletion of Mtarc1 on steatosis and fibrosis endpoints in several models of MASH in mice. The gene discussed is MTARC1; the disease is metabolic dysfunction-associated steatohepatitis.