Oligodendroglioma is the second most common malignant brain tumor in adults. Pathologically, oligodendrogliomas are categorized as grade 2 (low grade) or 3 (anaplastic) tumors. The median survival is 7–10 years for patients with low-grade oligodendrogliomas and 3.5 years for anaplastic tumors. The genetic hallmark of these tumors is an imbalanced translocation between chromosome 1 and 19 t(1;19)(q10;p10), resulting in loss of 1p and 19q. This codeletion is found in 50–70% of all oligodendrogliomas [1]. For years, scientists have searched for the basis of this unbalanced translocation. Unlike most translocations found within tumors, such as the Philadelphia chromosome, where the translocation results in an activated oncogene, the t(1;19) (q10;p10) occurs in gene poor peri centromeric regions. As a result, it was postulated that the biological basis for the translocation is a mechanism for unmasking tumor suppressor gene(s) via the loss of 1p/19q. Candidate gene approaches, like those used prior to the advent of current sequencing and genomic technologies, have failed to identify the driving force behind this translocation [2–5].