This mini review summarizes cellular and spatial mechanisms by which myeloid states drive ICI non-response in CRC, emphasizing stromal TGF-β–coupled SPP1+ TAM programs, granulocytic chemokine axes (CXCL1/2–CXCR2; IL-8–CXCR1/2), and mregDC-mediated co-inhibition. The gene discussed is CXCL1; the disease is colorectal carcinoma.