In an in vitro model of CKD, endothelial cells exposed to serum from uremic patients decreased their expression of intercellular adhesion molecule (ICAM)-1 and increased the phosphorylation of p38 mitogen-activated protein kinase (p38MAPK)-NF-κB signaling, and EUK-118 and EUK-134 treatment significantly decreased both intracellular ROS and phosphorylated p38MAPK-NF-κB expression [139]. The gene discussed is NFKB1; the disease is chronic kidney disease.