Observations from studies of different cellular and mice models of AD show that overexpression and hyperphosphorylation of tau impair localization and distribution of mitochondria (Ebneth et al., 1998; Kopeikina et al., 2011; Shahpasand et al., 2012; Rodríguez-Martín et al., 2013), which further cause defects in axonal function and loss in synapses (Cabezas-Opazo et al., 2015; Wang et al., 2015). The gene discussed is MAPT; the disease is Alzheimer disease.