Leptin, an adipocytokine elevated in NAFLD patients, exerts profibrogenic effects during the progression from NAFLD to NASH and also operates as a proangiogenic mediator through the recruitment and stabilization of hypoxia-inducible factor 1-alpha (HIF-1α) and the nuclear translocation of HIF. Here, HIF1A is linked to metabolic dysfunction-associated steatotic liver disease.