According to the Nephroseq database (www.nephroseq.org, University of Michigan, Ann Arbor, MI) (13), hypoexpression of METTL3, METTL14 and WTAP has been reported in diabetic mice, in patients with chronic kidney disease (CKD) and patients with focal segmental glomerulosclerosis, indicating the feedback disruption of m6A. It has been demonstrated that METTL14-induced m6A methylation could posttranscriptionally modulate Sirt1 mRNA, contributing to podocyte injury(14). This evidence concerns the gene METTL3 and chronic kidney disease.