In Met-dependent cell lines such as MKN45 (gastric cancer) and EBC-1 (LC), FGFR is a key regulator of resistance to a Met-targeting antibody.18 In acute myeloid leukemia, FGFR1 activity is required for the compensatory upregulation of hepatocyte growth factor in response to Met inhibition.19 Furthermore, hepatocyte growth factor secretion compensates for cancer cell growth inhibition by BGJ398, a selective FGFR inhibitor.20 This evidence concerns the gene HGF and acute myeloid leukemia.