FGFR2 and neoplasm: The hypothesis of FGFR2c involvement in EMT and consequently in early tumor development is also strengthened by the interesting findings of Oltean and coworkers [16] which, using an in vivo model of epithelial tumor progression, demonstrated that the inactivation of the FGFR2 splicing machinery, and consequently the aberrant appearance of FGFR2c, is associated to mesenchymal/EMT phenotype in primary tumor cells, while its restoration, which drives to FGFR2c down-regulation in favor of FGFR2b reappearance, is correlated with the epithelial/MET phenotype observed in micrometastases.