CMS1 tumor epithelial cells showed increased enrichment of immunological, proteasome, JAK-STAT and PD-1 signaling pathways, whereas CMS4 tumor epithelial cells displayed epithelial-mesenchymal transition (EMT), VEGF, and TGF-β activation, among other pathways (Fig. 2B) [10]. The gene discussed is SOAT1; the disease is neoplasm.