Accordingly, the downregulation of citronellol to NF-κB and AP-1 expressions in the current study could clarify the substantial anti-inflammatory role of citronellol in targeting upstream events that resulted in NF-κB and AP-1 activation through TLR4/MyD88, which is dependent on CLP-induced AKI [46]. The gene discussed is NFKB1; the disease is acute kidney injury.