To date, contrasting results were achieved in the preclinical application of tazemetostat; while it seemed to be completely ineffective in an in vitro model of H3.3 mutated glioma cells, it reduced the proliferation of glioma cells with H3 or IDH1/2 wild-type background; however, when the same cells were treated for prolonged period, it induced a shift in cell commitment, accelerating tumor progression through an induction of cell proliferation and DNA damage repair [133,134,135,136]. Here, IDH1 is linked to central nervous system cancer.