ARHGEF2 and colorectal carcinoma: Our bioinformatics analysis and in vitro and in vivo experiments showed that DMTN inhibited the activity of Rac1 by interacting with ARHGEF2, but the downregulation of DMTN relieved the binding to the ARHGEF2 protein and then enhanced Rac1 signaling pathway activity, stimulated lamellipodia and protrusion formation, and promoted the CRC cell metastasis.