In 3xTg-AD mice that overexpress mutant Swedish APP (AD causal mutation), MAPT P301L and Presenilin M146V (AD causal mutation), a DYRK1A benzimidazole-like inhibitor reversed cognitive deficits via decreasing Aβ42 aggregation and decreasing phosphorylation of insoluble Tau (Branca et al., 2017). The gene discussed is APP; the disease is Alzheimer disease.