Studies that have addressed GSK-3β activation in diabetic animal models (using antibodies detecting the phosphorylation state either at the Ser9 inhibitory site, or the Tyr216 activation site of the kinase) have shown contradictory findings (Table 1), thus making it difficult to conclude about the implication of this kinase in the correlation between diabetes and Tau pathogenesis. The gene discussed is MAPT; the disease is diabetes mellitus.