Proinflammatory cytokines subsequently activate key transcription factors such as STAT3 (signal transducer and activator of transcription) or NF-κB (nuclear factor kappa B) in premalignant lesions, and these mechanisms promote other malignant processes, such as cell proliferation, angiogenesis, or metastasis, and maintain the inflammatory tumor microenvironment. This evidence concerns the gene NFKB1 and neoplasm.