Elevated TG levels in HTG-AP lead to more free fatty acids released during pancreatic lipase hydrolysis than in AP induced by other causes [21], contributing to the development of systemic inflammatory response syndrome (SIRS) and progression to hyperlipidemic severe acute pancreatitis (HLSAP) [10, 22], with more severe pancreatic necrosis later in the course of the disease. This evidence concerns the gene PNLIP and alkaline phosphatase measurement.