The pro-oncogenic effects of STAT3 are mostly evident following inactivation of the negative regulators of IL-6 signaling, such as the suppressor of cytokine signaling 3 (SOCS3), that leads to an increased phosphorylation of protein kinase B (AKT), and NF-κB, initiating the disease process in patients that will progress towards IBD-CRC (Johnson et al., 2018). This evidence concerns the gene NFKB1 and inflammatory bowel disease.