Multiple cancer- and immune-related pathways were associated with the risk model, such as the VEGF, Toll-like receptor, TGF-β, T cell receptor, Nod-like receptor, MAPK, JAK-STAT, and B cell receptor, base excision repair, DNA replication, citrate cycle, pentose phosphate pathway, protein export, nonhomologous end joining, selenium amino acid metabolism, ribosome, steroid biosynthesis, RNA polymerase, mismatch repair, endometrial cancer, and these pathways were enriched in the high-risk group. This evidence concerns the gene SOAT1 and endometrial cancer.