Recent research demonstrates that TFEB overexpression and small‐molecule TFEB activators can attenuate NLRP3‐driven inflammation in AD animal models, indicating that targeting ALP—particularly through master regulators TFEB and TFE3—may suppress neuroinflammation and mitigate HFD‐induced metabolic and cognitive impairments [47]. The gene discussed is TFE3; the disease is Alzheimer disease.