Several mechanisms contribute to hypoalbuminemia in acute pancreatitis, including (i) an energy deficit due to fasting and increased tissue catabolism, (ii) inflammatory cytokine-mediated suppression of hepatic albumin synthesis, and (iii) cytokine-induced endothelial dysfunction, leading to increased capillary permeability and albumin leakage into the interstitial space [43]. This evidence concerns the gene ALB and acute pancreatitis.