There may be several pathways by which this subtype of enzyme of the AKR subfamily affects NAFLD progression: (i) reduced protection against oxidative stress due to increased aldose reductase activity and increased advanced glycation end-products [28]; (ii) low intracellular level of retinoic acid due to AKR1B10-mediated reduction of retinaldehyde to retinol [12,29]; and (iii) reduced production of natural peroxisome proliferator-activated receptor-γ ligands via the diversion of prostaglandin (PG) D2 toward PG F2α and away from PG J2 [30]. Here, AKR1B1 is linked to metabolic dysfunction-associated steatotic liver disease.