Another study reported the overexpression of METTL14 reversed high-glucose-activated phosphatidylinositol-3-kinase/protein kinase B(P13K/Akt) pathway inactivation in HK2 by enhancing phosphatase and tensin homolog (PTEN), followed by the downregulation of histone deacetylase 5 (HDAC5), thus ameliorating DN manifestations such as fibrosis, inflammation, cell death, and albuminuria (32, 49). Here, AKT1 is linked to liver dysplastic nodule.