To confirm these in silico findings experimentally, we stimulated primary renal epithelial cells (RPTECs) with TNF, which is central to CKD progression31,32 and which activates both the AP-1 and NF-κβ pathways33,34, and performed a CUT&RUN assay to determine binding sites of NF-κβ1 and JUN (Fig. 7f, Supplementary Fig. S21). The gene discussed is TNF; the disease is chronic kidney disease.