Recent studies have found that after continuous stimulation by intracellular and extracellular factors, the MAPK/ERK pathway is over activated and the activated ERK activates many downstream effector molecules, such as NF-κB, RSK, and others, which can cause proliferation, survival, and angiogenesis of tumor cells and the transcription of different genes related to metastasis.29–31. This evidence concerns the gene NFKB1 and neoplasm.