Although it is not resolved if activated HCSs could potentially contribute to galectin-3 expression in NASH models with less advanced inflammation and fibrosis, liver samples from AMLN ob/ob-NASH mice show highly different distribution of α-SMA and galectin-3 immunostaining (data not shown), which argues for HSC-derived galectin-3 expression being neglectable in this model. This evidence concerns the gene ACTA1 and metabolic dysfunction-associated steatohepatitis.