Amyotrophic lateral sclerosis (ALS) is characterized by progressive motor neuron degeneration leading to muscle atrophy [100, 101, 102], with pathogenesis involving mitochondrial accumulation of mutant SOD1 protein [103], glutamate excitotoxicity‐induced Ca2+ overload and mitochondrial ROS burst [104], as well as protein homeostasis disruption and neuroinflammatory cascades [105, 106], where the AMPK/SIRT1/PGC‐1α pathway plays a dynamic regulatory role (Table 1). The gene discussed is PRKAA1; the disease is amyotrophic lateral sclerosis.