There is growing evidence that the impairment of mitochondrial function due to abnormal MPTP opening is a critical event in all studied types of acute pancreatitis.[4, 20] The resulting amplification cascade of events, such as reduced ATP production, defective autophagy, zymogen activation, cytokine release, and the activation of phosphoglycerate metastable enzyme family member 5 (PGAM5), leads to an increasingly intense inflammatory response and ultimately to pancreatic necrosis. The gene discussed is PGAM5; the disease is acute pancreatitis.