In some settings, engagement of PRR by bacterial components results in a pro-tumorigenic environment, e.g. F. nucleatum, through TLR4 activation, has been shown to mediate M2 polarisation, promoting a proinflammatory, pro-tumour microenvironment [71]. Both F. nucleatum and ETBF can also induce infiltration of myeloid cells into the tumour microenvironment, promoting an immunosuppressive, pro-tumourigenic microenvironment [68, 69], with M2 tumour-associated macrophages associated with poor prognosis [70]. This evidence concerns the gene TLR4 and neoplasm.