Interestingly, the phosphorylation levels of CaMKII α/β were further reduced in both of the long-term STZ treatment groups (Fig. S3, A, D, E, F, I, and J), indicating that long-term hyperglycemia triggered impairment of neuroplasticity (13), which was not dependent on the existence of human tau. The gene discussed is CAMK2G; the disease is Hyperglycemia.