Lee et al. [56] have demonstrated that temozolomide (TMZ)-triggered HIF1α/HIF2α upregulation plays a critical role in converting non-stem glioma cells to acquire stem-like characteristics, and that knockdown of HIF1α/HIF2α suppressed the interconversion between non-stem glioma cells and GSCs post-therapy [56]. Here, EPAS1 is linked to glioma.