Since PARP is known to poly(ADP-ribosyl) ate itself as a mean of self-inactivation [27], in those cancers where PARG’s upregulation correlates with poor survival rate, an elevated level of PARG may be sufficient to keep PARP re-activated but, at the same time, may not be sufficient to reduce the overall level of pADPr and thus to suppress tumorigenicity. This evidence concerns the gene PARG and cancer.