These studies identified differential methylation to have a role in ADPKD via upregulation of SMYD2 contributing to renal cyst formation due to methylation of STAT3 and p65, subsequently resulting in increased renal cell proliferation [53], epigenetic silencing of PKD1 and other ion transport genes in ADPKD due to hypermethylation [52], and identification of reduced expression of MUPCDH as a prognostic biomarker of ADPKD [51]. The gene discussed is STAT3; the disease is autosomal dominant polycystic kidney disease.