Chen Y et al reported that catalpol could reduce the protein expression of MyD88 in mouse kidney podocytes induced by high glucose, interrupt the signaling of MyD88, and could not effectively activate NIK or phosphorylate IKK, which in turn failed to relieve the inhibitory effect of IκB on NF-κB and inhibit the nuclear transfer of NF-κB, thereby reducing the production of the downstream inflammatory factors IL-6, TNF-α, and IL-1β and improving DKD podocyte injury.[13] 7-Hydroxycoumarin is a derivative of coumarin, the active component of A sinensis and other traditional Chinese medicines. This evidence concerns the gene NFKB1 and diabetic kidney disease.