As opposed to the other classical tumor suppressors, C/EBPδ seems, however, neither hypermethylated, nor mutated, lost or deleted in pancreatic adenocarcinoma (re-analysis of previously published data [48,49,50]) suggesting re-activation of C/EBPδ may hold therapeutic promise in the setting of pancreatic adenocarcinoma. Here, CEBPD is linked to neoplasm.