Fusobacterium nucleatum infection and activating KRAS mutations form a self-reinforcing oncogenic loop in colorectal cancer: Fn virulence factors (FadA, Fap2, OMVs) stimulate Wnt/MAPK- and IL-6/IL-17-driven inflammation that enhances KRAS-dependent proliferation and drug resistance, while the KRAS-mutant epithelium reshapes the mucosal niche to favor persistent Fn colonization. Here, IL17A is linked to colorectal cancer.