It has been shown that Aβ1-42 can activate glycogen synthase kinase 3β (GSK3β), also formerly known as Tau protein kinase 1 (TPK1), which leads to the abnormal hyperphosphorylation of tau and formation of p-tau, which can polymerise and leads to the formation of PHFs and eventually NFTs; these processes further exacerbate AD pathology [28,30]. The gene discussed is MAPT; the disease is Alzheimer disease.