Recent transcriptomic analyses of treatment-naïve GCA lesions have identified macrophages and multinucleated giant cells expressing a wide array of molecules implicated in GCA pathogenesis, including MMP12 (critical for elastin degradation), ACP5 and ATP6V0D2 (osteoclast-associated bone resorption molecules), VDR and TREM2 (involved in osteoclastogenesis and phagocytosis), MRC1 (a marker of fibrosis-associated macrophages), and HLA-DRA (involved in antigen presentation to CD4+ T cells) [118]. Here, ELN is linked to temporal arteritis.