In inflamed synovia, NGF acting via TrkA–MEK/ERK–AP−1 augments ICAM−1 expression and promotes M1 polarization, illustrating that NGF can gate adhesion programs and macrophage state through canonical kinase cascades; analogous circuits are expected to operate in tumor-associated macrophages exposed to NGF−rich milieus (40, 41). The gene discussed is NTRK1; the disease is neoplasm.