In this situation our hypothesis is as follows: it is likely to be due to the increased arachidonic acid level during pancreatitis inhibiting the expression of ANGPTL8, and, secondly, due to the low level of ANGPTL8, LPL activity is less affected; accordingly, it may be possible that increased free fatty acids following further hydrolysis of TG may predispose to pancreatitis. This evidence concerns the gene LPL and pancreatitis.