In summary, our findings suggest that HIPK2-CT, generated by active-caspase-6, can act as a negative regulator of renal inflammation by inactivation of the NF-κB pathway in renal tubular cells and that HIPK2-CT peptide analogs could be potentially developed to modulate NF-κB and antiinflammatory response in CKD. This evidence concerns the gene NFKB1 and chronic kidney disease.