While many studies considered ACE primarily as an enzyme that could promote proteolysis of β-amyloid in vitro [16–18], recent experimental and clinical studies provide strong evidence that inhibition of ACE-dependent angiotensin II generation in vivo could actually reduce signs of neurodegeneration in experimental AD models [19, 20] and slow the cognitive decline of patients with Alzheimer's disease [21–25]. The gene discussed is AGT; the disease is Alzheimer disease.