These experiments suggest that (A) UFAs are the consequence of lipolysis of visceral fat by pancreatic lipases; (B) local UFAs produce necrosis of acinar pancreatic cells; and (C) uncontrolled UFA release results in high UFA levels in the bloodstream and is associated with renal tubular apoptosis (and subsequently with kidney failure) as well as with cell damage in lung alveoli that is similar to that seen in acute respiratory distress syndrome (6, 7, 9, 12, 22). Here, PNLIP is linked to acute respiratory distress syndrome.