Similarly, in the present study we demonstrated that TGF-β1 could increase SET7/9 occupancy at p21 gene promoter, and silencing SET7/9 with siRNAs could partly abolish TGF-β1-induced p21 gene upregulation in RMC, supporting that SET7/9-dependent H3K4me1 plays a key role in p21 expression and SET7/9 could be a strong preventive agent against RMC hypertrophy in CKD. The gene discussed is TGFB1; the disease is chronic kidney disease.