The inappropriate activation of STAT3 signaling pathways in tumor cells, alike NF-κB persistent activation, is not directly attributable to activating mutations in the genes encoding these transcription factors or the JAK/STAT pathway, although mutations in components of the signaling pathway such as gp130 and SOCS3, have been described in inflammatory liver tumours [52] and in lung cancer [53], respectively, resulting in STAT3 hyperactivation. This evidence concerns the gene NFKB1 and neoplasm.