NFKB1 and cancer: Instead of being functional inert, there is circumstantial evidence that CAFs are pro-inflammatory due to activation of nuclear factor kappa B (NF-κB), signal transducer and activator of transcription (STAT)-1 and−3, and transforming growth factor (TGF)-β/SMAD signaling and are engaged in active cross-talk with cancer cells (19, 20).