Dysregulated Wnt/β-catenin activity levels play a role in various disease processes.4 Epigenetic silencing ofSFRP1 elevates Wnt/β-catenin activity, which has been linked to cancer.2,4 Conversely, high concentrations of sFRP-1 suppresses Wnt/β-catenin activity, which is predicted to have implications in neurological diseases, such as Alzheimer’s disease (AD).1,3–5 Targeting sFRP-1 to restore the Wnt/β-catenin signalling pathway is of current interest in AD research to discover novel therapies.3 Mechanistic studies would be greatly facilitated with the availability of high-quality antibodies. The gene discussed is SFRP1; the disease is Alzheimer disease.