Mesenchymal cells generated by EMT form cell adhesion sites, that is, focal adhesions and/or podosomes/invadopodia, at which the Src-ARHGEF5-Rho axis is upregulated and activated.21 As ARHGEF5 can also function as a scaffold for PI3K,21 upregulated ARHGEF5 may activate Akt pathways, thereby promoting cell survival via the antiapoptotic pathway and cell growth via the mammalian target of rapamycin complex 1 pathway.39 Indeed, we observed that ARHGEF5-dependent activation of Akt was required for tumor growth from mesenchymal-like colorectal cancer cells. This evidence concerns the gene AKT1 and neoplasm.