Cell Division Autoantigen 1 (CDA1) has been shown to play a role in enhancing transforming growth factor beta (TGFβ) signaling, leading to fibrosis in diabetic kidney disease (DKD) using mouse strains with global CDA1 gene deletion. In these models, diabetes has been induced, leading to DKD in the absence of CDA1. It is still unknown whether inhibition of CDA1 activity after onset of diabetes in the presence of CDA1 can attenuate renal fibrosis in vivo. Thus, we examined the effect of inducing genetic deletion of CDA1 in adulthood in mice using a tamoxifen-activated estrogen receptor fused cyclization recombinase (ERCre)-Locus of cross-over in P1 (LoxP) system. Male mice at 6-8 weeks of age were rendered diabetic with streptozotocin (STZ) or injected with buffer alone to serve as non-diabetic controls. Five weeks later, genetic deletion of CDA1 was induced by tamoxifen administration in CDA1Flox/ERCre mice, with mice injected with vehicle to serve as CDA1 wildtype controls. Kidney tissues were analyzed 5 weeks after deletion of CDA1. Tamoxifen administration reduced CDA1 gene expression by ~80% in CDA1Flox/ERCre mice. Renal levels of phosphorylated Smad3 and expression of profibrotic genes as well as accumulation of extracellular matrix proteins (ECMs) such as collagens III and IV were increased in diabetic mice, and induced deletion of CDA1 led to attenuation of these parameters. Therefore, targeting CDA1 after onset of diabetes in mice where CDA1 was initially expressed is able to attenuate diabetes-associated renal injury, providing the impetus to target this pathway in order to reduce diabetic kidney disease.