SOAT1 and cancer: Specifically, the following pathways were significantly enriched in the high expression phenotype: ECM-receptor interaction, GAP junction, leukocyte transendothelial migration, the JAK-STAT signaling pathway, the MAPK signaling pathway, pathways in cancer, the TGF-β signaling pathway, the Toll-like receptor signaling pathway, the intestinal immune network for IgA production, and natural killer cell-mediated cytotoxicity (Figure 6K).