NFKB1 and neoplasm: CAFs are pro-inflammatory due to activation of nuclear factor kappa B (NF-κB), signal transducer and activator of transcription (STAT)-1 and STAT-3, and transforming growth factor (TGF)-β/SMAD signaling and are thereby engaged in active cross-talk with cancer cells through paracrine signaling involving chemokines, prostaglandins (PGE), insulin-like growth factor (IGF), and proteases [26,27,28,29,30,31], thereby promoting tumor angiogenesis, growth, and aggressiveness.