While VASH-1 expression is suppressed during DKD progression, its residual activity may partially restrain TGF-β1/Smad3-driven fibrosis, as VASH-1 depletion exacerbates renal damage via unchecked TGF-β1 signaling and amplifies oxidative stress through dysregulated SIRT1/HIF1-α pathways [118]. The gene discussed is VASH1; the disease is diabetic kidney disease.