Numerous cytokines, growth factors, and intracellular signaling molecules, such as non-coding RNAs, are released during pancreatitis to regulate PSC activation; however, accumulating evidence points to a major role for interleukin-6 (IL-6) and transforming growth factor β (TGF-β) in modulating the persistent activation and fibrotic phenotype of PSCs in vitro and in vivo. The gene discussed is IL6; the disease is pancreatitis.