Defying the generalized conclusion that bevacizumab does not impact survival in GBM, Japanese investigators uncovered a survival benefit for bevacizumab in MGMT-unmethylated, CDKN2A-deficient GBM,13 plausibly by blocking autocrine stimulation through the vascular endothelial growth factor (VEGFA)–KDR–PI3K pathway.14 Mechanistically, MTAP is also synthetic lethal with GARFT. This evidence concerns the gene CDKN2A and glioblastoma.