There was a complex mutual regulation between hypoxia and inflammation,[51,52] and Chen et al validated that tubular epithelial cells exposed to hypoxia would incite tubulointerstitial inflammation.[53] In all, these indicated that TwHF might activate PI3K-Akt signaling pathway as well as TNF signaling pathway to progress renal inflammation, mediate hypoxia via HIF-1 signaling pathway to accelerate inflammatory processes. This evidence concerns the gene HIF1A and inflammatory response.