Also in this model, BAI repaired T1DM-induced renal injury partly through modulating Klotho promoter methylation (a well-recognized endogenous inhibitor against renal fibrosis), as well as suppressing epithelial-to-mesenchymal transition (EMT) and microRNA-124/TLR4/NF-κB axis to repair renal fibrosis (Zhang S. et al., 2020; Zhang X. T. et al., 2020). This evidence concerns the gene TLR4 and renal fibrosis.