Martinez et al. (2017) found that hsa-miR-125b-5p and hsa-miR-16 could regulate the expression of TJ genes CGN and CLDN2, respectively, and negatively correlated with defecation pattern and the frequency of abdominal pain. Recently, one study reported that hsa-miR-219a-5p was able to change intestinal barrier function and visceral hypersensitivity through neuron and MAPK signaling, so it was expected to be a potential therapeutic target for IBS (Mahurkar-Joshi et al., 2021), strongly supporting the thesis of our study. This evidence concerns the gene CLDN2 and irritable bowel syndrome.