Several substrates wereidentified, including steroids (e.g., estradiol) and other bioactivelipids (e.g., leukotriene B4), using an in vitro enzyme assay system in which NAD+ (nicotinamide adeninedinucleotide, oxidized form) acted as co-substrate.7 Thus, numerous lines of evidence suggest HSD17B13 is apromising target for pharmacological treatment of NASH. This evidence concerns the gene HSD17B13 and metabolic dysfunction-associated steatohepatitis.