Furthermore, studies employing transcriptomic analyses of GCA and non-inflamed aortic tissues revealed an enrichment of interferon (I, II and III) signatures and JAK/STAT signalling in GCA.88 89 Pharmacogenomic network analysis also identified IFN-γ and CXCL10 to be druggable candidate genes.89 It is however noteworthy that disease duration prior to surgery is not specified for this cohort and the representative GCA-aortic cohort was relatively small.89 The gene discussed is SOAT1; the disease is temporal arteritis.