Additionally, though the phosphorylation levels of JNK and p38 in the cortex of WT mice were not severely affected by STZ treatment (Fig. S3, A–C), we speculated that the transient activation of JNK by hyperglycemia may be sufficient for triggering tau phosphorylation at certain residues as seen in Figures 1G and S1D. This evidence concerns the gene RNF19A and Hyperglycemia.