Using aldolase as a target, we identified an inhibitor termed aldometanib, which specifically prevents the v-ATPase-associated aldolase, but not the cytosolic aldolase involved in glycolysis, from binding to FBP even under high glucose, thereby mimicking a state of low glucose to activate AMPK via the lysosomal pathway.38 Depletion of factors involved in the lysosomal pathway in the liver, such as LAMTOR1 and AXIN, inhibits aldometanib-mediated activation of AMPK.38 In an AMPK-dependent manner, aldometanib alleviates hyperglycemia, fatty liver, and NASH in obese rodents.38 The gene discussed is PRKAA2; the disease is Hyperglycemia.