AD is associated to extracellular deposition of amyloid-β (Aβ) plaques due to an increased production and/or lack of clearance of Aβ peptides derived from amyloid precursor protein (APP) cleavage (Mawuenyega et al., 2010; Sarlus and Heneka, 2017) and by abnormal intraneuronal accumulation of hyperphosphorylated tau protein (Johnson and Stoothoff, 2004) (Figure 1). The gene discussed is APP; the disease is Alzheimer disease.