Increased DYRK1A also phosphorylates APP and promotes pathological processing of APP into neurotoxic Aβ peptides (Ferrer et al., 2005; García-Cerro et al., 2017; Arbones et al., 2019), overexpressing DYRK1A mice displaying AD pathology including neurodegeneration, disrupted synaptic plasticity and memory (Ferrer et al., 2005; Ahn et al., 2006; Liu et al., 2008; García-Cerro et al., 2017). The gene discussed is APP; the disease is Alzheimer disease.