In both HALLMARK and KEGG database, the high-risk group showed enrichment not only in classical oncogenic signaling pathways (e.g. KRAS, JAK-STAT, and P53 signaling pathways) and tissue remodeling-related pathways (e.g. myogenesis and ACTIN cytoskeleton pathways) activated to facilitate tumor growth, but also demonstrated significant enrichment in inflammation and immune response-related pathways, including IFN-γ response and TNF-α signaling pathways. The gene discussed is SOAT1; the disease is neoplasm.