A previous study reported that the hematopoietic depletion of CYP27A1 and thus the inhibition of 27-HC synthesis in another murine NASH model with knockout of low-density lipoprotein receptor (Ldlr−/−) and an HFD feeding for 12 weeks resulted in stronger NASH activity upon CYP27A1 depletion compared with wild-type controls. This evidence concerns the gene VLDLR and metabolic dysfunction-associated steatohepatitis.