By studying the functional activity of FPR1 in GC experimental models, we described that the genetic ablation of FPR1 in human GC cells expressing high levels of the receptor increased their angiogenic and tumorigenic potential in vivo; accordingly, enforced expression of FPR1 in GC cells expressing low FPR1 levels caused the opposite effect, drastically impairing angiogenesis and tumor growth in vivo (Prevete et al., 2015b). This evidence concerns the gene FPR1 and neoplasm.