Dysregulated Ca2+ levels in the pancreatic acinar cells are fundamental to the pathogenesis of pancreatitis by causing premature activation of PRSS1 (Krüger et al., 2000), ER stress (Sah et al., 2014) or hampered zymogen granule trafficking in the acinar cells (Messenger et al., 2014). The gene discussed is PRSS1; the disease is pancreatitis.