Model for priming of genes for differential expression during CIP.

Under normal conditions, genes that promote pancreatic disease are silent while those that protect against injury are either active or primed for activity based on H3K4Me3 enrichment. Following exposure to a chronically injured environment (i.e. loss of MIST1), these genes become reprogrammed so that the response to an adverse environmental challenge now leads to the activation of genes promoting disease progression and severity. This model includes potential epigenetic silencing mechanisms to the DNA or histones, which were not investigated in this study.