Using NIH3T3 clones that express either wild-type or kinase-inactive mutant forms of FGFR2-KCTD1 or FGFR2-TXLNA, the Nakamura et al. showed that wild-type FGFR fusions, and not the mutant forms induce tumor growth in vivo via ligand-independent autophosphorylation and activation of the MAPK signaling pathway. Here, FGFR2 is linked to neoplasm.