This study investigates the role of *Fusobacterium* spp., particularly *Fusobacterium nucleatum*, in intestinal tumorigenesis. The authors found that *Fusobacterium* spp. are enriched in human colonic adenomas and stool samples from colorectal adenoma and carcinoma patients compared to healthy subjects. In mouse models of intestinal tumorigenesis, *F. nucleatum* increased tumor multiplicity and recruited specific myeloid cells, leading to a pro-inflammatory microenvironment. This pro-inflammatory signature was also observed in human colorectal carcinomas with high *Fusobacterium* abundance. Unlike other bacteria linked to colorectal cancer, *F. nucleatum* did not exacerbate colitis or inflammation. The findings suggest that *Fusobacterium* spp., particularly *F. nucleatum*, contribute to colorectal neoplasia progression by modulating the tumor immune microenvironment through the recruitment of myeloid-derived immune cells.This study investigates the role of *Fusobacterium* spp., particularly *Fusobacterium nucleatum*, in intestinal tumorigenesis. The authors found that *Fusobacterium* spp. are enriched in human colonic adenomas and stool samples from colorectal adenoma and carcinoma patients compared to healthy subjects. In mouse models of intestinal tumorigenesis, *F. nucleatum* increased tumor multiplicity and recruited specific myeloid cells, leading to a pro-inflammatory microenvironment. This pro-inflammatory signature was also observed in human colorectal carcinomas with high *Fusobacterium* abundance. Unlike other bacteria linked to colorectal cancer, *F. nucleatum* did not exacerbate colitis or inflammation. The findings suggest that *Fusobacterium* spp., particularly *F. nucleatum*, contribute to colorectal neoplasia progression by modulating the tumor immune microenvironment through the recruitment of myeloid-derived immune cells.