[13] It has been proposed that the fusion, which occurs via a tandem duplication event, leads to loss of an miR-99a binding site within the 3′-untranslated region (3′- UTR) of FGFR3, releasing FGFR3 signaling from miR-99a-dependent inhibition and enhancing tumor progression relative to wild type FGFR3. [22] Given the close proximity of the FGFR3 and TACC3 genes, identification of the fusion by FISH is technically challenging. The gene discussed is TACC3; the disease is neoplasm.