This speculation is supported by our findings that PPARβ/δ was functionally expressed in human glomerular mesangial cells, where its activation and overexpression markedly enhanced basal and IL-1β-induced COX-2 expression and PGE2 production, which may accelerate glomerulonephritis by promoting the biosynthesis of the proinflammatory chemokines and cytokines responsible for the recruitment of leukocytes from circulation to the glomeruli. The gene discussed is IL1B; the disease is glomerulonephritis.