Moreover, several studies have demonstrated that DcR3 functions as an effector molecule in various cells, independently of the FasL/Fas pathway, by regulating migration and invasion abilities (10,11), ERK stimulation in gastric cancers (41), increasing adhesion in monocytes via PI3K/Akt activation (17) and regulating proliferation and migration of HUVECs via MMP-2 regulation (12). This evidence concerns the gene FAS and gastric cancer.