By combining top ten network analysis with a search for PPAR responsive elements, we identified the platelet-derived growth factor (PDGF)/platelet-derived growth factor receptor (PDGFR) pathway, tyrosinkinase KIT (c-Kit), and the VEGF/vascular endothelial growth factor receptor (VEGFR) pathway as mediators of the pro-angiogenic tumor promoting effect of PPARβ/δ [29]. The gene discussed is KIT; the disease is neoplasm.