Glioblastoma Multiforme (GBM) is the most common and malignant primary brain tumor in humans. Unfortunately, it remains almost uniformly fatal. Despite standard treatment involving respective surgery, radiation therapy, and temozolomide, recurrence of GBM is inevitable, and patients with recurrent GBMs have limited treatment options. In 2009, bevacizumab was approved for the standard treatment of recurrent GBM. Bevacizumab (BEV) is an anti-angiogenic monoclonal antibody that acts as a Vascular Endothelial Growth Factor (VEGF) inhibitor. In this project, genetic data from 119 Glioblastoma Multiforme patients were assessed and correlated to outcomes following BEV treatment. Gene mutations in IDH1, BLM, and PRKDC were shown to be associated with longer therapeutic effects of BEV, while those of TP53, PTEN, EGFR, ERCC5, and SF3B1 were associated with less effect of BEV. Additionally, the chromosomal arms 2p and 2q were significantly amplified (extra copy(s) of all the genes in these regions of the DNA) in patients whose disease was progressing at the first follow-up exam after starting BEV, while 19p was amplified in those who exhibited partial response. Our goal is to be able to use these and any genetic marker identified in future studies to predict which patients will benefit most and which will not respond to BEV treatment.