For example, STAT3 could inhibit glial tumor growth downstream of mutations of PTEN, but not of type III epidermal growth factor receptor (EGFRvIII) [42]; help bypass senescence in prostate cancer [43]; suppress tumor development by impairing the expression of IL-8 and thus the recruitment of myeloid cells in kirsten rat sarcoma viral oncogene homolog (K-RAS) mutant lung adenocarcinomas [44]; impair tumor progression in APC mutant colon cancer but not in inflammation-driven colorectal carcinogenesis [45,46,47,48]; and impair tumor cell proliferation in thyroid carcinomas [49]. This evidence concerns the gene CXCL8 and neoplasm.