The m6A RNA methyltransferase METTL3 can enhance TUG1 mRNA stability and expression by IGF2BP2 to restore HG-induced renal tubular mitochondrial dysfunction, suggesting that upregulation of METTL3 or IGF2BP2 as possible upstream mechanisms for TUG1 may serve as candidate therapeutic strategies for mitochondria bioenergetics in DN through promoting trancription of PGC-1α. Here, IGF2BP2 is linked to liver dysplastic nodule.