In this context, it was evident from these studies that telomere shortening and activating mutations in KRAS are among the more frequent and early events in pancreatic carcinogenesis; these gene abnormalities are followed at later stages of tumor development by inactivating mutations of the p16 (CDKN2A) tumor suppressor and in the TP53 and SMAD4 tumor suppressor genes. The gene discussed is CDKN2A; the disease is neoplasm.