It recruits tumor associated macrophages (TAMs) and dendritic cells (DCs), depletes T cells, reduces FoxP3 regulatory T cell enrichment, and dampens NK cell activity, suppressing anti-tumor immunity and exacerbating pro-inflammatory CRC mechanisms.100–102 On the one hand, it enhances M2 macrophage polarization (ARG-1, IL-10, MRC1, TGF-β) and CCL20 expression via NF-κB/miR-1322, facilitating CRC metastasis.103 On the other hand, it activates ALPK1-mediated NF-κB, upregulating ICAM1 to promote CRC adhesion, extravasation, and metastasis to the endothelium.104. This evidence concerns the gene TGFB1 and neoplasm.