Further, CSF was found to mitigate DN by targeting NF-κB-mediated inflammation, which ameliorated podocyte foot process effacement and albuminuria, alleviated the injury of glomerular and tubular, as well as extracellular matrix accumulation in STZ-induced diabetic rats through decreasing the expression of NF-κB, p65, a1-chain type IV collagen, MCP-1, ICAM-1, and TNF-α [54,74]. The gene discussed is NFKB1; the disease is liver dysplastic nodule.