Does ALR deficiency pave the way for NASH progression

We read with interest the recent paper by Kumar et al. (1), on the impact of ALR deficiency on nonalcoholic fatty liver disease (NAFLD) progression from steatosis to nonalcoholic steatohepatitis (NASH). By using hepatocyte-specific ALR knock-out /down high fat/high carbohydrate mouse models they demonstrated an involvement of ALR in lipid metabolism, oxidative stress, inflammatory response leading to fibrosis. However, ALR is expressed in three isoforms (15, 21/23 kDa) (2) and their specific roles in this "loss-of-function" strategy is not addressed.