Because CCK is a major physiological regulator of pancreatic acinar cell function (Jensen, 1994; Chandra and Liddle, 2007; Williams, 2019), and is also important in pathophysiological models of pancreatitis (Gukovskaya et al., 2002), we subsequently concentrated our studies on CCK’s effect on activation of cofilin and the signaling cascades involved. This evidence concerns the gene CFL1 and pancreatitis.