Dyrk1 inhibition rescued the observed cognitive deficits in 3xTg‐AD mice with a concomitant reduction in Aβ and τ pathology136 via decreasing phosphorylation of both APP and insoluble τ, thereby increasing APP metabolism and decreased Aβ levels.137 DYRK1A phosphorylates τ on 11 different Ser/Thr residues many of which are found in NFTs of AD,116 and its overexpression led to increased 3R‐τ and decreased 4R‐τ.138 This is mediated through influence on the alternative slicing of τ exon 10.139, 140 Inhibition of Dyrk1A by Leucettine L41141 or EHT 5372142 mitigated both τ and Aβ pathologies. The gene discussed is APP; the disease is Alzheimer disease.