Further findings included broader upregulation of lipid catabolism and mitochondrial metabolism, including mitochondrial enzymes (e.g., Acsf2, Acadl, and Acaa2) with NVS‐PAK1‐1 treatment across all cohorts suggesting a metabolic rebalancing toward fatty acid oxidation and mitochondrial efficiency may help mitigate metabolic dysfunction common in AD, though the direct connection to PAK1 inhibition is uncertain. The gene discussed is PAK1; the disease is Alzheimer disease.