PC arises from precursor lesions called pancreatic intraepithelial neoplasms (PanINs), which are characterized by the sequential accumulation of alterations in the K-ras oncogene and loss of the CDKN2A, p53, and/or SMAD4 tumor suppressors along with upregulation of pro-survival Bcl-2 [17]. The gene discussed is BCL2; the disease is neoplasm.