The SIRT1 regulatory network influences cellular aging processes and modulates stress/inflammatory responses in neurodegeneration [111], exerting protective effects in ALS through FOXO/PGC‐1α deacetylation to enhance antioxidant capacity (increased SOD2 activity) and activation of autophagy pathways for misfolded protein clearance (improved aggregate removal) [112, 113], with SIRT1 overexpression shown to mitigate SOD1 mutation‐induced ALS pathology [112]. The gene discussed is SOD1; the disease is amyotrophic lateral sclerosis.