Confirming the role of a defective T regulatory response in GCA, two studies recently demonstrated that GCA patients had a Treg compartment enriched in IL-17 secreting a Treg (Th17-like Treg) with an impaired suppressive capacity, which was mainly related to the expression of a hypofunctional isoform of FoxP3 lacking exon 2 (FoxP3Δ2), which is required for the antagonization of RORγt and RORα, the main transcriptional factors controlling the production of IL-17 [101,142]. The gene discussed is IL17A; the disease is temporal arteritis.