As shown in GO analysis, the potential targets of SZF acting on DKD were mainly associated with various biological processes, such as lipopolysaccharide-mediated signaling pathway, inflammatory response, positive regulation of cyclase activity, protein kinase B signaling, positive regulation of MAP kinase activity, and response to estradiol, which had a strongly direct correlation with the pathogenesis of DKD [32–38]. The gene discussed is AKT1; the disease is diabetic kidney disease.