In the specific setting of GCA, two cytokine clusters apparently drive the inflammatory process: (a) the steroid-sensible IL-6/IL-17 cluster, which would be sustained by Th17 cells; and (b) the IL-12/interferon gamma cluster due to the persistent activity of Th1 cells, responsible for the progression or refractoriness of the disease despite corticosteroid or anti-IL-6 drugs [13]. The gene discussed is IL6; the disease is temporal arteritis.