In addition, elevated METTL3 levels within podocytes initiate m6A modification of tissue metalloproteinase inhibitor (TIMP)2 mRNA, subsequently facilitating direct interaction between the m6A reader IGF2BP2 and the TIMP2 mRNA m6A site, consequently leading to podocyte dysfunction in DKD.53 Here, IGF2BP2 is linked to diabetic kidney disease.