PPARβ/δ expression was significantly higher in human colorectal cancers compared to adenomatous polyps and normal mucosa [50] and also in the malignant cells—invasive front versus their paired tumor centers and adenomas—and proinvasive pathways (connexin 43, PDGFRb, AKT1, EIF4G1 and CDK1) were upregulated in response to PPARβ/δ stimulation [17]. The gene discussed is PPARD; the disease is neoplasm.