Data from experiments in 3 × Tg-AD and Tg-SwDI mice indicated that ablating M1 mAChR promoted tau hyperphosphorylation and amyloidogenic processing, which were attributed to changes in PKC and GSK-3β activities, as well as increasing the astrocytic and microglial response associated with Aβ plaques (Medeiros et al., 2011). The gene discussed is MAPT; the disease is Alzheimer disease.