In a study investigating their role in GCA, Ly KH et al. reported an enhanced expression of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), tropomyosin receptor kinase B (TrkB), and sortilin in GCA temporal arteries compared to control arteries that also express these molecules to a lesser extent [182]. Here, NTRK2 is linked to temporal arteritis.