Overexpression of CK1ε suppressed tau exon 10 inclusion and increased the phosphorylation of tau at multiple pathological epitopes in cultured cells and in mouse brain, which suggests that up-regulation of CK1ε may contribute to tau pathology in AD brain via dysregulation of phosphorylation and exon 10 splicing of tau and thus represents a promising target for therapeutic intervention. This evidence concerns the gene MAPT and Alzheimer disease.