Therefore, gastric epithelial STAT3 may contribute to cancer initiation; however, JAK/STAT signaling in gastric epithelial cells, Stat3 expression in stromal cells, and/or other signaling pathways (e.g., the JNK and NF-κB signaling pathways) may contribute to gastric tumorigenesis [38, 39]. The gene discussed is SOAT1; the disease is cancer.