Li and colleagues were able to show that HIF2A expression correlates with both increased TIC properties and poor glioma patient survival [47], and a follow-up study further specified that HIF2A, in a feed-forward loop together with hypoxia-induced histone methyltransferase mixed-lineage leukemia 1 (MLL1), acts to drive TIC self-renewal and glioma initiation [48]. Here, KMT2A is linked to glioma.