Then, we generated mice with podocyte-specific deletion of PVT1 (Nphs2-Cre/Pvt1flox/flox) and confirmed that the deletion of PVT1 suppressed podocyte mitochondrial dysfunction and inflammation in addition to ameliorating diabetes-induced podocyte injury, glomerulopathy, and proteinuria. The gene discussed is PVT1; the disease is diabetes mellitus.