CYCS and alkaline phosphatase measurement: Although numerous factors can contribute to AP, the over‐generated mitochondrial reactive oxygen species (mtROS) is a pivotal factor in its complex pathogenesis.[7] Excessive mtROS leads directly to mitochondrial breakage and triggers cytochrome c (Cyt c)‐mediated apoptosis of pancreatic acinar cells (PACs).[8] Furthermore, macrophage activation during AP is strongly associated with the overproduction of reactive oxygen species (ROS).[9] Macrophages hold a central position in the AP inflammatory response.