As shown in figure 3A, B and online supplemental figure S1, JAK2 and STAT5A, the main signalling proteins activated by GM-CSFR engagement, were phosphorylated in GCA lesions, and transcripts regulated by STAT5, such as Spi1 (PU.1) and CD83, were significantly increased in GCA arteries (figure 3C–G). The gene discussed is STAT5A; the disease is temporal arteritis.