In contrast, another study demonstrated that the deletion of VDAC2 in rodent glioblastomas and colorectal tumors inhibited BAX-mediated apoptosis and worsened the response to chemotherapy, suggesting that VDAC2 may be essential for activating BAX-mediated apoptosis and limiting the growth of these tumors (24). This evidence concerns the gene VDAC2 and glioblastoma.