Although AD is a complex disease with several pathogenic mechanisms, this work focuses on the importance of the DYRK1A hyperexpression, since the increased expression of this enzyme leads to hyper-phosphorylation of Tau protein and APP, which results in high levels of Aß peptide (leading to β-amyloidosis) and aggregation of Tau protein, and subsequent formation of neurofibrillary tangles [9]. The gene discussed is DYRK1A; the disease is Alzheimer disease.