Indeed, mouse models and clinical data clearly indicate important AD enhancing roles for the DYRK1A kinase (because of its ability to directly phosphorylate tau, APP and RCAN1) [90,91,92], RCAN1 (a calcium regulated phosphatase able to increase tau-phosphorylation through inhibition of the phosphatase calcineurin and to regulate vesicle fusion kinetics) [93,94], ETS2 (a transcription factor upregulated by oxidative stress that transactivates APP) [95,96,97] and BACE2 (a non-amyloidogenic θ-secretase) [98,99,100]. The gene discussed is RCAN1; the disease is Alzheimer disease.