Paradoxically, different studies have described an increased expression of FGF21 in the liver and white adipose tissue of DIO mice and obese humans, as well as in conditions such as hypertension, atherosclerosis, and MASLD [42,44,45]; additionally, ER stress in the liver has also been shown to be a contributor to FGF21 expression, which may activate mechanisms such as augmented ketogenesis, gluconeogenesis, and lipolysis to regulate the liver’s homeostasis [46]. The gene discussed is FGF21; the disease is metabolic dysfunction-associated steatotic liver disease.