NGF is released by cells when tissues are damaged and causes pain by binding to Tropomyosin receptor kinase A (TrkA) on nociceptors and inflammatory cells, leading to transmission of pain signals28. NGF levels are increased in synovium of patients with advanced OA compared to non-OA controls, and in patients exhibiting symptomatic chondropathy compared to asymptomatic patients31, suggesting a potential role for NGF in the pathogenesis of OA pain32. The gene discussed is NGF; the disease is cartilage disease.