JAK2 and metabolic dysfunction-associated steatotic liver disease: Nordstrom and colleagues demonstrate this important principle, showing that adipocyte-specific deletion of JAK2 almost completely reverses the NAFLD phenotype in mice with hepatocyte-specific deletion of JAK2, proving that GH-stimulated adipocyte lipolysis is necessary for the steatotic phenotype seen in mice with liver-specific GH signaling defects [59].