Accordingly, dysbiosis induced by antibiotics inhibited the clinical benefit of ICB in patients with advanced cancer (13), which could be restored by administration of different bacterial taxa; in this respect, particularly relevant was the association of improved tumoricidal activity with the accumulation of CD4+ T cells expressing the small intestine–associated chemokine receptor 9 (CCR9) and the T helper 1–associated chemokine receptor CXCR3 in mesenteric lymph nodes (mLNs), tumor-draining LNs, and tumor beds of mice gavaged with A. muciniphila after antibiotic treatment (10). This evidence concerns the gene CCR9 and cancer.