In addition, another report demonstrated that the elimination of HDAC11 enhances mitochondrial fatty acid oxidation by activating the AMPK pathway and reducing intracellular carnitine levels in skeletal muscle, consequently improving muscle strength and fatigue resistance.[33] Therefore, it is hypothesized that the inhibition of HDAC11 may exert its anti‐MASLD effects through the activating AMPK in the liver. This evidence concerns the gene PRKAA2 and metabolic dysfunction-associated steatotic liver disease.