Although the molecular mechanism functionally linking Aβ42 to Tau, as well as its contribution to the pathophysiological mechanism behind AD progression, remains under extensive study, it was reported that Aβ42 increased pTau and that GSK3β inhibition blocked the increased pTau and prevented Aβ42-induced impairment of LTP in mice [9]. The gene discussed is GSK3B; the disease is Alzheimer disease.