Our results indicated that trypsin co-expressed with PAR2 in the pancreatic tissues neither from the patients with CALCB mutations nor that of the wild-type, it maybe supporting the effects of trypsin in the AIP.6, 7 These findings are in agreement with previous data demonstrating that ectopic trypsinogen activation can directly stimulate the inflammation in the pancreas.6, 7 Moreover, trypsin and tryptase acting on PAR-2 receptors, stimulate the release of neuropeptides from slices of the spinal cord (Supplementary Fig. 2). This evidence concerns the gene F2RL1 and autoimmune pancreatitis.