Another study reported that an ER stress inhibitor inhibits lipopolysaccharides (LPS)-stimulated CD206 production in macrophages.24 In cancers, the pro-tumor functions of TAMs promote the expression of cell surface receptors, cytokines, chemokines, and enzymes, in addition to activating Treg cells or suppressing other effector cells.25 Inhibition of IRE1α-XBP1 in macrophages may attenuate CD86 and PD-L1 surface expression.26 Therefore, targeting XBP1 pathway of TAMs may be a novel strategy for CRC immunotherapy. This evidence concerns the gene CD177 and neoplasm.