Indeed, we show that HSCs express both NPR-B and NPR-C and previous multiomic studies in both murine models of MASLD and human hepatic tissue suggest that multiple cell types in the liver express NPRs, including endothelial cells, fibroblasts, and hepatocytes (43, 44), implying that a multimodal effect of CNP, through both cognate NPRs on several cell types, is likely to underpin the salutary actions of the peptide in MASLD. This evidence concerns the gene NPR2 and metabolic dysfunction-associated steatotic liver disease.