In vitro and in vivo functional studies show that MYB-QKI rearrangements promote tumorigenesis through three mechanisms: MYB activation by truncation, enhancer translocation driving aberrant MYB-QKI expression and hemizygous loss of the tumor suppressor QKI.     ///    MYB-QKI rearrangements in angiocentric glioma drive tumorigenicity through a tripartite mechanism..     ///    We identified MYB-QKI fusions as a specific and single candidate driver event in angiocentric gliomas. 