There are several described mechanisms of methionine dependency of cancer cells, including mutations in 5-methyltetrahydrofolate-homocysteine methyltransferasegene MTR (present in approximately 8% of cancer samples), deletions in methyl-thioadenosine phosphorylase gene MTAP (found in approximately 15% of cancer samples including melanoma and pancreatic cancer [12,13]), and low levels or complete absence of methionine synthase [3,14,15]. Here, MTR is linked to familial pancreatic carcinoma.