Herein, CU06-1004, whose efficacy and safety have been established previously in preclinical disease models related to endothelial dysfunction, was established as a vascular leakage blocker; its principal mode of action appears to be mediated by anti-inflammatory effects based on suppressing NF-κB activation and by anti-permeability effects occurring through activation of the small GTPase Rac and translocation of cortactin in ECs11,12. The gene discussed is NFKB1; the disease is endothelial dysfunction.