In vitro experiments have shown that TLR4 activation can promote the polarization of macrophages towards the M1 phenotype via the TLR-4/MyD88/NF-κB pathway.368 Furthermore, in a mouse model of peritoneal carcinomatosis of colorectal cancer, a high-fat diet was found to promote M1 polarization of adipose tissue macrophages (ATMs) by activating TLR4. Here, MYD88 is linked to colorectal cancer.