Hu et al. (2017) reported that lncRNA-MALAT1 expression is enhanced in renal tissues of STZ-induced DN compared with normal renal tissues. HG treatment also results in the increase of MALAT1 expression in podocytes. They further demonstrated that knockdown of MALAT1 inactivates Wnt/β-catenin signaling and protects against HG-induced podocyte injury. More important, MALTA1 inhibition restores podocytes function by the mediation of Wnt/β-catenin signaling (Hu et al., 2017). This evidence concerns the gene MALAT1 and liver dysplastic nodule.