In malignant cells and/or cells bearing oncogenic mutations, interleukins, such as IL-6, IL-11, and IL-22, stimulate STAT3 signaling that upholds cell proliferation, survival, stemness, epithelial–mesenchymal transition (EMT), and migration [46]; excessive STAT3 activation driven by IL-6 and IL-11 overexpression combined with oncogenic driver mutations mediate the development of solid tumors (e.g., lung, pancreatic, colon and gastric cancer) [46]. This evidence concerns the gene STAT3 and gastric cancer.