Thus, further work is needed to elucidate the role, and function of PLAGL2 in tumor angiogenesis, which could provide not only evidence-based mechanisms of GBM-acquired resistance to anti-angiogenic treatment but also a proof of concept for translational research by combining anti-angiogenic therapy to effectively eradicate GBM, thus constituting a landmark clinical advance for GBM. This evidence concerns the gene PLAGL2 and glioblastoma.