SIRT1 and cancer: In all cases, CAP-mediated tNOX inhibition is causally related to a decline in the intracellular NAD+/NADH ratio and subsequent increases in the generation of extramitochondrial oxidative stress, which, in addition to affecting the proliferative potential, negatively affects the activity of the coenzyme NAD+-dependent deacetylase sirtuin-1 (SIRT1) and configures a transductional arrangement that occurs selectively in cancer cells.