In GCA lesions, the transmural inflammation of affected arterial walls ultimately results in the formation of granulomas with MGCs, wherein abundant numbers of IFN-γ-activated macrophages stimulate the induction and production of pro-inflammatory cytokines, chemokines, reactive oxygen species, matrix metalloproteinases, and growth factors, of which the later essentially comprise vascular endothelial growth factor (VEGF), PDGF, and transforming growth factor beta (TGF-β). The gene discussed is IFNG; the disease is temporal arteritis.