In addition to the strategy of attempting to block 2-HG production, there is an alternative therapeutic strategy exploiting the biological consequences of mutant IDH by targeting the 2-HG-dependent homologous recombination deficiency that renders IDH-mutant glioma cells sensitive to poly (adenosine 5’-diphosphate-ribose) polymerase (PARP) inhibitors. The gene discussed is PARP1; the disease is central nervous system cancer.