This hypothesis is consistent with – yet not proven by – findings of increased GSK3 activation in 2 different models of Aβ-induced Tau-pathology that we have analyzed[52, 55], and with the fact that inhibition of GSK3 using adeno-associated-viral-mediated knock-down in a model with combined amyloid and Tau-pathology could reduce the latter[113]. The gene discussed is MAPT; the disease is amyloidosis.