The identified proteins are involved in several pathways already identified in the pathophysiology of GCA, such as inflammation (interleukin [IL]1 beta, IL-6, IL-8, IL-23, IL-31, interferon gamma, etc.), vascular involvement (vascular endothelial growth factor, intercellular adhesion molecule 1), or monocyte/macrophage involvement (macrophage receptor with collagenous structure, macrophage colony stimulating factor, chitinase 3-like protein 1, also known as YKL-40). This evidence concerns the gene IL23A and temporal arteritis.