This growing list of phosphorylation sites affected by DYRK1A, which now includes key sites regulating microtubule affinity (T231, S262) [19], [20] and references therein], tau toxicity (T231, S262, T212) [21], and sites hyperphosphorylated coincident to NFT pathology (S396, S404) [22] suggest that DYRK1A could be a critical regulator of tau function and dysfunction during the course of AD. This evidence concerns the gene MAPT and Alzheimer disease.