In GCA-arteries, VSMC dysfunction has been observed in response to mitogenic signals such as PDGF.22 GCA-TAs show transmural PDGF expression, predominantly at the media-intima junction, with levels correlating with intimal hyperplasia and clinical ischaemia.72 In-vitro studies demonstrated that PDGF induced the proliferation and migration of GCA-derived VSMCs.22 In line with this, imatinib (a tyrosine-kinase inhibitor inhibiting PDGF receptor activity) decreased myointimal cell proliferation, outgrowth, as well as production of collagen I/II and fibronectin in ex-vivo GCA models.22 Here, FN1 is linked to temporal arteritis.