Genetic alterations of the malignant cells of GBM also involve the inactivation of tumor suppressor genes (PTEN, P16, RB, and TP53) [12,13,14], promoting cell proliferation due to a down-regulation of apoptosis by an increase in the levels of anti-apoptotic proteins (Bcl-2, Mcl-1, Bcl-xL, HIAP-1, HIAP-2, and XIAP) and a decrease in pro-apoptotic proteins (Bid, Bak, Bax, Bad, Bim, PUMA, NOXA, caspases-8, -10, -9, Apaf, DR4, Fas, and FADD) [15,16,17,18,19,20]. Here, BCL2L1 is linked to glioblastoma.