SMAD4 and colorectal carcinoma: We previously demonstrated that aberrations in TGF-β signaling caused by SMAD4 deficiency promoted the expression of mouse CCL9, or human CCL15 (a human ortholog of mouse CCL9) from CRC cells to recruit CCR1+ myeloid cells (TANs and MDSCs) within primary and metastatic CRCs [7–12].