Collectively, these data support a dual role for C3G in lymphoma, stemming from both altered activity and expression: hyperactivated C3G functions as a tumor suppressor by inhibiting cell proliferation and promoting apoptosis through Rap1-dependent inhibition of the Raf-ERK1/2 pathway, while concurrently reducing adhesion—likely via downregulation of Rac2 activation—thereby enhancing migration and invasion. This evidence concerns the gene RAPGEF1 and neoplasm.