Huang et al. reported that Beclin-1 overexpression in cell gliomas decreased cell viability by inducing apoptosis [133]; the authors propose that Beclin-1 binds and inactivates Bcl-2 and Bcl-xL, allowing the activation of the pro-apoptotic proteins Bax and Bak, which open permeability transition pores, releasing mitochondrial cyt c into the cytosol and subsequently activating caspase-9 and -3, suggesting that Beclin-1 regulates cell death processes like apoptosis and autophagy by binding members of the Bcl-2 family [133] (Figure 5 and Figure 6). This evidence concerns the gene BAK1 and glioma.