Exposure of endothelial cells (ECs) to sera from CKD patients results in morphological alterations, enhanced thrombogenicity of the extracellular matrix and changes towards a pro‐inflammatory phenotype, with increased expression of adhesion receptors and activation of signalling pathways, such as nuclear factor‐kappa B (NFkB),10 or the innate immunity Toll‐like receptor 4 (TLR4) and the NALP3 inflammasome.11 Moreover, the endothelial response to the CKD insult is also characterized by an enhanced oxidative stress and changes in the expression of related proteins.12, 13, 14, 15. This evidence concerns the gene NFKB1 and chronic kidney disease.