We know that flagellated bacteria and hematopoietic TLR5+ cells at mucosal surfaces are driving differential tumor progression because: 1) depletion of commensal bacteria with a non-absorbable cocktail of antibiotics abrogates any TLR5-dependent differences in tumor growth; 2) and reconstitution of TLR5+ mice with TLR5-deficient (but not TLR5+) bone marrow recapitulated the delayed progression of syngeneic and autochthonous tumors observed in TLR5 KOs. The gene discussed is TLR5; the disease is neoplasm.