Cholesterol, as a major component of lipid rafts, is thought to be involved in amyloid precursor protein (APP) processing and β-amyloid (Aβ) overproduction characterized as a key feature of AD pathophysiology [12], while gemfibrozil, a fibric acid agent commonly used to treat hyperlipidemias in clinic, significantly reduces amyloid pathology and reverses memory deficits in APP-PSEN1ΔE9 mice [15], a murine model that mimics AD-like pathology and cognitive decline. The gene discussed is APP; the disease is hyperlipidemia.