Using a series of in vitro experiments, in vivo animal models, liquid chromatography–tandem mass spectrometry (LC–MS/MS), and chromatin immunoprecipitation (ChIP), we show that CRIP1 can reshape the tumor microenvironment by increasing secretion of vascular endothelial growth factor C (VEGFC) and C‐C motif chemokine ligand 5 (CCL5) from GC cells. The gene discussed is VEGFC; the disease is neoplasm.