The upregulation of UGCG may increase Gb3 availability, while the coordinated upregulation of GLA may prevent Gb3 accumulation in persons with DKD not having Fabry disease, but in Fabry disease, a lack of GLA activity may result in further Gb3 accumulation in patients with coexistent diabetes and, in the case of missense genetic variants, in the accumulation of abnormal GLA proteins that may cause endoplasmic reticulum stress. This evidence concerns the gene GLA and Fabry disease.