High levels of Mcl-1 mediate BH3-mimetic resistance, suggesting that a dual inactivation of Bcl-2/Bcl-xL and Mcl-1 is necessary for apoptosis of glioblastoma cells (Kouri et al., 2012; Karpel-Massler et al., 2017; Shang et al., 2020). This evidence concerns the gene BCL2L1 and glioblastoma.