We were also able to confirm that the mutual interactions between MFAP5 + fibroblasts and tumor-infiltrating myeloid cells prompt malignancy by activating pro-tumorigenic signaling pathways, such as the MIF/CD74 and IL34/CSF1R axes in myeloid cells, as well as enhancing the aggressive phenotypes of MFAP5 + fibroblasts through EGF and VISFATIN signals in a positive loop. This evidence concerns the gene MIF and neoplasm.