Ontology revealed that enhancer CpGs from the normal group are weakly associated with pathways commonly linked tumorigenesis (e.g., EMT and renal carcinoma signaling), unlike the tumor enhancer CpGs that were enriched for cancer-associated pathways like MAPK, PTEN, and CXCR4 signaling (Fig. 3H) [32, 33]. The gene discussed is PTEN; the disease is neoplasm.