Alternatively, a recent study aimed to achieve NAD depletion in IDH-mutant cancer cells, not by interfering with NAD synthesis but by blocking the regeneration of the mono ADP-ribose moieties from poly(ADP-ribose) (PAR) through the inhibition of poly(ADP-ribose) glycohydrolase (PARG), the enzyme responsible for PAR breakdown, with the simultaneous enhancement of PARP-mediated NAD consumption via DNA-damaging agents administration. This evidence concerns the gene PARP1 and cancer.