A higher NQO1 content in human malignancies has been linked to a higher burden of free radicals and redox imbalance (described later); however, the killing of pancreatic cancer cells after the inhibition of NQO1 by dicoumarol and other compounds [33,34,35,36,37,38] suggests the operation of off-target effects through multiple mechanisms. This evidence concerns the gene NQO1 and familial pancreatic carcinoma.