Although much of the currently-developed therapeutic approaches for AD target Aβ or Tau [8,9] and mut-Htt for HD [10], this review aims to impress upon the reader that the neuropathological action of these proteins requires or is regulated by the three kinases that the review focuses on and makes the case for targeting these kinases, possibly in combination with approaches that are currently being clinically tested, such as genetic knockdown or immunotherapy. The gene discussed is MAPT; the disease is Huntington disease.