Finally, mesenchymal-state GBM, which is frequently therapy resistant and may exhibit a higher anti-apoptotic threshold in part through differential Bcl-2 family programs (e.g., enrichment of BCL2A1 reported in mesenchymal GBM and IDH-wildtype settings), provides a plausible mechanism by which the Bcl-2:beclin-1 checkpoint could be biased toward autophagy-permissive survival rather than apoptosis [98]. This evidence concerns the gene BCL2 and glioblastoma.