To highlight this, De Strooper and Karran describe a “cellular phase” of AD, which follows a “biochemical phase” characterized by amyloid beta accumulation and tau hyperphosphorylation (Strooper et al., 2016), in which each cell-type has a unique phenotype invested with a profile of mechanisms which react and contribute to disease pathogenesis (Strooper et al., 2016). This evidence concerns the gene MAPT and Alzheimer disease.