Receptor tyrosine kinase (RTK)/RAS alterations occur frequently in gastric cancer and lead to the definition of five distinct gastric cancer subgroups characterized by genomic alterations in FGFR2, KRAS, EGFR, ERBB2/HER2 and MET, suggesting that approximately 37% of patients may potentially be treatable by RTK/RAS-directed therapies [3]. The gene discussed is FGFR2; the disease is gastric cancer.