Furthermore, the intercellular IL-23p19 peptide, produced in endothelial cells in GCA and promoted by pro-inflammatory factors (LPS, TNF-α and IFN-γ), stimulates the gp130-dependent activation of STAT3 by its association with the cytokine receptor subunit gp130, thus leading to an increase in intercellular adhesion molecules at the cell surface. The gene discussed is IFNG; the disease is temporal arteritis.