Using isolated pancreatic acini and in vivo models of acute pancreatitis, our group has shown that Substance P stimulates the formation of pro-inflammatory chemokines by a Ca2+, protein kinase C (PKC-δ), extracellular-signal-regulated kinase (ERK), S locus receptor kinase (SRK), and nuclear factor kappa B (NF-κB) dependent pathways [46,47]. The gene discussed is NFKB1; the disease is acute pancreatitis.