These models exhibited a decrease in zymogen granules, ER distention, and increased apoptosis in the pancreatic acini, leading to pancreatic degeneration.[29, 30, 31] Additionally, Sec23b hemizygosity (Sec23bki/ko) mice (ki, knocked in p.E109K mutation—the most common human mutation in congenital dyserythropoietic anemia type II patients; ko, knockout) displayed phenotypes consistent with CP.[32] These findings underscore the critical role of ER‐to‐Golgi transport in the pathogenesis of pancreatitis. The gene discussed is PSME3; the disease is Congenital dyserythropoietic anemia type II.