By blocking apoptosis and p53 signaling and redirecting the death program to necrosis, the molecular profile of Bcl2L12 provides a rational molecular explanation for hallmark features of GBM—that is, apoptosis resistance, florid necrosis, and soaring proliferation—and points to Bcl2L12 upregulation as a key progression event in malignant glioma. Here, BCL2L12 is linked to glioblastoma.