A new study of 97 tumours has demonstrated that a small proportion (3.1%) of glioblastoma multiforme brain tumours exhibit a chromosomal translocation that fuses the tyrosine kinase domain of fibroblast growth factor receptors 1 and 3 (FGFR1 and FGFR3) to the transforming acidic coiled-coil domains of TACC1 and TACC3, respectively. This results in a constitutively expressed fusion kinase that localizes to the mitotic spindles and induces mitotic defects and aneuploidy. Furthermore, the fusion protein induced oncogenic activity when transduced stereotactically in mouse brains. Interestingly, inhibition of FGFR kinase activity in a mouse model harbouring the same translocation corrected the aneuploidy, which suggests that the corresponding treatment might benefit patients with glioblastoma multiforme bearing the translocation.