Second, differences in thresholds might arise when the analysis is based on any DR as opposed to diabetes-specific DR. In other words, a microaneurysm could be caused by other pathologies besides diabetes. Third, we analyzed total DM participants including type 1 and type 2 DM together. However, because the number of type 1 DM was too small, and the number were statistically insignificant, we have included and analyzed DM type I and II participants aged 19 and over. Actually the statistical results were same using only the data of type 2 DM participants. Fourth, using proteinuria greater 1+ is a limitation. It does not adequately investigate the relationship of DR with urinary protein excretion, but in this version of cross-sectional study, we could not get more information from the urine analysis. Fifth, we could not get the data of drugs, which could affect the assessment of CKD and proteinuria as ACE inhibitors or angiotensin II receptor blockers. Despite these limitations, this study used a nationally representative sample of adults in Korea, which is a crucial strength. Additionally, we assessed all of the DM population 19 years and older. Moreover, to the best of our knowledge, this is the first large population based study to examine the association between DR and CKD and its components among a representative Korean diabetic population. Taken together, CKD appear to be associated with DR and VTDR in a Korean DM population. In particular, proteinuria, not decreased eGFR, is more significantly associated with DR or VTDR in diabetic patients. Ubiquitin-specific protease, a subfamily of deubiquitinating enzymes , is responsible for the removal of ubiquitin or polyubiquitin from target proteins, the processing of ubiquitin precursors, and the disassembly of unanchored polyubiquitin by catalyzing the hydrolysis of isopeptide bonds in ubiquitin-protein conjugates. USPs have been implicated in wide variety biological processes and involved in the pathogenesis of numerous diseases, including cancer and neurodegeneration. Recent studies found that USP have also been associated with neurogenetic disorders, including Parkinson��s disease and spinocerebellar ataxia. The tail suspension and forced swimming tests are useful experimental paradigms for assessing antidepressant activity and depression-like behavior. In the tests, animals are subjected to inescapable stress of being suspended by their tail or being forced to swim in a water-filled cylinder. The animals rapidly adopt a characteristic immobile posture that has been named ��behavioral despair�� on the assumption that the animals have given up hope of escaping. Recent study identified USP46 as a AZD152 Abmole SIX3, a tumor suppressor, inhibits astrocytoma tumorigenesis by transcriptional repression of AURKA/B quantitative trait gene responsible for the immobility in the tail suspension and forced swimming tests in mice. In this study, mice with a lysinecodon deletion of USP46 showed loss of ��behavioral despair�� under inescapable stresses in addition to abnormalities in circadian behavioral rhythms and the GABAergic system. The authors demonstrate that USP46 functions to regulate several behavioral processes, including basal immobility, the antiimmobility effects of imipramine, nest building and the muscimol-induced righting reflex. However, comparing the detailed description of the phenotypes of USP46 mutant mice, the molecular mechanism have not been well documented. In particular, whether the lysine codon deletion in USP46 affects deubiquitinating enzyme activity is unknown.