Their secretion is dysregulated in MASLD, where the increased leptin levels activate JAK2-dependent signaling pathways in the liver, through the binding to its receptor Ob-Rb in different hepatic cells, e.g., hepatocytes, Kupffer cells, and hepatic stellate cells, thus contributing to MASLD progression to MASH and fibrogenesis [64,65,66]. The gene discussed is LEP; the disease is metabolic dysfunction-associated steatotic liver disease.