Although we cannot discard the role of other cell types residing in the liver different than hepatocytes and HSCs, the low expression of GLP1R and GIPR in hepatic cell types (according to datasets), makes it unlikely that those cell types could be responsible for the entire beneficial effects of the GLP-1R/GIPR dual-agonism in people with MASH. Here, GLP1R is linked to metabolic dysfunction-associated steatohepatitis.