STAT3-enhanced activation in CRC occurs from IL-6 in the serum and the tumor microenvironment, from growth factors and growth factor receptors, tyrosine kinases (Src, Bcr-Abl), and loss-of-function mutations for the STAT3 suppressors/inhibitors (phosphatases, SOCS, PIAS) [35]. The gene discussed is STAT3; the disease is neoplasm.