Additionally, we unmasked the mechanism underlying the promotive role of OGT in CKD-associated VC and found that OGT overexpression enhanced KEAP1 glycosylation at the S104 site leading to degradation of the NRF2 transcription factor, which concurrently restricted VSMC autophagy and accelerated VSMC calcification, as reflected by elevated Runx2 and reduced α-SMA expression levels. The gene discussed is ACTA1; the disease is chronic kidney disease.