The main findings are that DM and Fabry disease may interact resulting in the modulation of kidney Gb3 synthesis pathways that may increase Gb3 availability through increased expression of UGCG, the gene encoding the upstream and rate-limiting enzyme glucosylceramide synthase, and limit the recruitment of compensatory kidney protective genes, potentially causing more severe inflammation and accelerated kidney failure. Here, UGCG is linked to diabetes mellitus.