Catecholamines, for example, have been shown to activate macrophages via adrenergic signaling, leading to a shift towards the M2-polarized phenotype and increased VEGF production, which ultimately promotes tumor angiogenesis.326,327 This catecholamine-driven effect was found to be mitigated by the β-AR antagonist, propranolol. The gene discussed is VEGFA; the disease is neoplasm.