Although the signal transduction of IL-6 is crucial for STAT3 activation in CRC initiation and development [63,67,68,69], the ablation of STAT3 in intestinal enterocytes has more significant effects on mucosal damage and regeneration, tumor growth, and proliferation than the lack of IL-6 in the CAC model induced by AOM and DSS [68], indicating that other cytokines involved in STAT3 activation, such as EGF family growth factors, IL-11, and IL-22, as well as hormones, such as leptin, may drive the activation of STAT3 in inflammation-induced CRC cells. This evidence concerns the gene STAT3 and colorectal carcinoma.