Stimulation of preferred long-patch BER leads to genomic maintenance while stabilization of intermediate DNA-structures or CAG repeats can lead to development of tumor cells or neurodegenerative processes [73] In a pancreas-specific HMGB1-deficient mouse model, intracellular HMGB1 limited nuclear damage and nucleosome release, leading also to milder clinical symptoms in acute pancreatitis [76]. This evidence concerns the gene HMGB1 and acute pancreatitis.