Nonetheless, a study revealed highly proliferative (Ki-67+) α-SMA+ cells to be enriched in the adventitia and intima of vasculitis-induced human arteries engrafted in SCID mice.96 Their proliferative activity significantly decreased on Tofacitinib (JAK1/3 inhibitor) treatment, with a notable reduction in intimal hyperplasia.96 Together, these data suggest that fibroblasts in GCA-arteries are likely activated in the adventitia, migrate towards the intima, and contribute to the intimal myofibroblast population and intimal hyperplasia. This evidence concerns the gene ACTA1 and temporal arteritis.