Differences in results from administration of XMU-MP-1 in AD mice with regards to YAP activation suggest that while acute treatment with XMU-MP-1 appears sufficient to ameliorate cognitive deficits without affecting YAP transcriptional output [16], longer treatment regimes produce alterations in YAP localization or activity [15, 19], which carries increased possibility of off-target effects. The gene discussed is YAP1; the disease is Alzheimer disease.