Competing models of the sporadic Alzheimer's disease (AD) cascade have debated whether the two primary pathologies, amyloid-beta (Aβ) plaques and tau neurofibrillary tangles, are causally related, with some suggesting that early amyloid pathology drives later tau pathology and others suggesting both pathologies arrive through distinct, unrelated molecular pathways (Small and Duff, 2008; Jack et al., 2010, 2013). The gene discussed is MAPT; the disease is Alzheimer disease.