Consistently, overexpression of MALAT1 enhanced HG-induced ROS generation, secretion of inflammatory cytokines, and cell apoptosis, and in vivo knockdown of MALAT1 through intravenous injection of a lentivirus expressing sh-MALAT1 alleviated renal tubular epithelial injury by suppressing LIN28A and the Nox4/AMPK/TOR signaling in rats with DN [104]. This evidence concerns the gene MALAT1 and liver dysplastic nodule.