TNF‐α was applied as it is a well‐defined and major inflammatory cytokine in the pathogenesis of IBD, and is linked to compromised goblet cell responses and mucus barrier dysfunction in IBD.1, 10 During TNF‐α challenge S. thermophilus CCFM218 and L. rhamnosus CCFM237 significantly potentiated transcription of sulfotransferase GAL3ST2, which makes these two strains promising candidates for promoting mucin sulfation and strengthening mucus barrier. The gene discussed is GAL3ST2; the disease is inflammatory bowel disease.