The ability to dimerize TACC3 leads to the presence of a constitutively dimerized, and thereby activated, FGFR3 tyrosine kinase domain in fusion-positive tumor cells and hyperactivated downstream signaling, resulting in an overexpression of phosphorylated FRS2, the initial intracellular binding partner of FGFR3, to activate ERK1/2 and AKT signaling [20,22,27,40,68]. This evidence concerns the gene TACC3 and neoplasm.