Studies focusing on the mechanisms of F. nucleatum-associated colorectal cancers have revealed that the influence of tumourigenesis is not exerted by inducing inflammation or exacerbating colitis-associated colorectal cancer; rather, it is conducted by increasing the infiltration of CD11b+ myeloid cells, a phenotype of myeloid-derived suppressor cells (MDSCs) in mice, which facilitate tumour growth and angiogenesis 127,128. This evidence concerns the gene ITGAM and colorectal cancer.