1,25(OH)2D3 activates VDR in ECs to suppress pro-inflammatory pathways like NF-κB, reducing cytokines (IL-6, TNF-α) and improving endothelial nitric oxide synthase (eNOS) activity, which mitigates sepsis-induced vascular leakage and oxidative stress [262]. Here, NFKB1 is linked to Sepsis.