By administering CBM 588 to CDI-infected mice, Hayashi et al. demonstrated that (1) butyrate produced by CBM 588 acted as an antibiotic peptide for Reg3βγ, (2) butyrate-induced neutrophils were not only induced through GPR43/109a signaling but also by metabolites besides butyrate, and (3) Th1 and Th17 cells are induced by butyrate-mediated GPR43/109a signaling [67] (Figure 1). The gene discussed is FFAR2; the disease is clostridium difficile infection.