Sun exposure has been associated with lower death rates for pancreatic cancer in ecological studies. Skin exposure to solar ultraviolet B radiation induces cutaneous production of precursors to 25-hydroxy (OH) vitamin D (D) and is considered the primary contributor to vitamin D status in most populations. Pancreatic islet and duct cells express 25-(OH) D 3-1α-hydroxylase that generates the biologically active 1,25-dihydroxy(OH) 2 D form. Thus, 25(OH)D concentrations could affect pancreatic function and possibly pancreatic cancer etiology. Serum 25-(OH)D is the major circulating vitamin D metabolite and is considered the best indicator of vitamin D status as determined by the sun and diet. Although recent prospective epidemiologic studies of higher predicted vitamin D status score and vitamin D intake and pancreatic cancer risk suggest protective associations, a nested case-control study showed a significant 3-fold increased risk for pancreatic cancer with higher vitamin D status. Limitations of these studies include the former do not measure vitamin D status on pancreatic cancer cases and the later was conducted in a male smoker population. More research is needed, particularly examination of pre-diagnostic vitamin D status and risk of pancreatic cancer, prior to conclusions for vitamin D's potential role in the etiology of this highly fatal cancer.