Moreover, PAR2 regulates the gastrointestinal motility and secretion and may play a vital role in autoimmune disease.20, 25 The trypsin released during inflammation and injury cleave and activate PAR2 on the terminals of nociceptive spinal afferent neurons and directly act on these receptors in eliciting inflammation and pain by means of neurogenic pathways.26, 27 The release of these inflammatory mediators are consequences of the complex interplay of PI3K/ERK1/2 kinase.28 Therefore, we explored the possible involvement of CALCB mutations in the trypsin-induced AIP. This evidence concerns the gene CALCB and autoimmune disease.