According to the amyloid cascade hypothesis, which is a key event in the initiation of AD, soluble amyloid β accumulation into toxic oligomers and amyloid plaques initiates a pathogenic cascade leading to accumulation of the hyperphosphorylated tau protein in neurofibrillary tangles, reduced numbers of synapses, death of neuronal cells, mitochondrial malfunction, and eventually loss of cognitive function (Drachman, 2014). The gene discussed is MAPT; the disease is Alzheimer disease.