Taken together, these data implicated DNMT1 in the maintenance of SST epigenetic silencing in pancreatic adenocarcinoma and supported the contribution of 5-AZA-mediated DNMT1 inactivation, which could be responsible for the demethylation of the SST promoter and SST reexpression in epigenetically reprogramed PANC-1 cells. The gene discussed is SST; the disease is pancreatic adenocarcinoma.