In the context of gliomas, tumours with IDH1/2 mutations may exhibit a ‘BRCAness’ phenotype as a consequence of inhibition of HR DNA repair processes by the enhanced levels of oncometabolites, which could explain why a subset of IDH‐mutant tumours respond well to conventional DNA damaging chemotherapies such as temozolomide as well as PARP1 and ATR inhibitors [141, 143, 144]. Here, PARP1 is linked to neoplasm.