The majority of SNVs in FGFR have been reported to occur in FGFR2 and are found at high frequencies in endometrial cancer (12%), non-small cell lung cancer (4%) and gastric cancer (4%).1,19,20 Interestingly, these somatic-activating FGFR2 mutations predominantly occur in the transmembrane (Y375C, C382Y/R) and extracellular domains (S252W, W290C, P253R) rather than the kinase domain (N549H/K, K659E).3 Extensive in vitro and in vivo analyses of these mutations have revealed that their oncogenic potential is due to increased receptor–ligand binding affinity and receptor dimerisation. The gene discussed is FGFR2; the disease is gastric cancer.