Others have shown that the loss of the 3′ untranslated region of FGFR3 allows the fusion to escape miR-99a regulation in glioblastoma; additionally, the TACC3 fusion partner induces mitotic defects by recruiting endogenous TACC3 away from the mitotic spindle, where TACC3 is canonically required for providing stabilization [6, 7]. The gene discussed is TACC3; the disease is glioblastoma.