Increasing evidence implicates CRMP2 in the pathogenesis of AD [3,4,5,6], where dysregulated phosphorylation mediated by hyperactive kinases such as glycogen synthase kinase-3β (GSK-3β) and cyclin-dependent kinase 5 (Cdk5) contributes to disease-associated cellular abnormalities [7,8,9,10]. This evidence concerns the gene CDK5 and Alzheimer disease.