The activation of nuclear factor-κB (NF-κB) by TNF-α and IL-1β as well as the activation of signal transducer and activator of transcription (STAT)3 by IL-6 in a tumor microenvironment could potentiate colonic inflammation, induce uncontrolled cell proliferation, and further promote CRC progression (Waldner et al., 2012; De Simone et al., 2015; Voronov and Apte, 2015; Lin et al., 2020). The gene discussed is NFKB1; the disease is neoplasm.