Furthermore, in DLD-1 cells, we supplemented recombinant MIF concomitantly with ectopic CD74 which mimics paracrine MIF-CD74 interactions to induce VEGF and IL8. In the in vivo CRC model, we assume that tumor epithelial cells do both, secrete MIF to recruit macrophages to the tumor (which consequently secrete angiogenic factors) (Fig. 4B); and provide an autocrine MIF-CD74 interaction to induce the MAPK-VEGF axis (Fig. 5B and F), albeit we have not specifically tested it in this study. The gene discussed is CD74; the disease is colorectal carcinoma.