Inflammatory mediators, such as tumor necrosis factor (TNF-a), CXC ligand 1 (CXCL1), and CXCL2, are increased by the remaining unbuffered non-esterified UFAs, that inhibit mitochondrial complexes I and V, reducing ATP levels: this mechanism contributes to the pancreatic necrosis, thus worsening acute pancreatitis [51, 53]. The gene discussed is TNF; the disease is acute pancreatitis.