By PLA we could demonstrate, indeed, colocalization of the IL-12/IL-23p40 and IL-12p35 subunits configuring IL-12 and colocalization of IL-12/IL-23p40 and IL-23p19 subunits conforming IL-23 in GCA, supporting the participation of both Th1 and Th17 differentiation pathways in the development of arterial inflammation. The gene discussed is IL23A; the disease is inflammation.