This study, through the combined application of network pharmacology and untargeted metabolomics, revealed the AGE-RAGE and PI3K-Akt pathways as significantly altered in response to HLB treatment, leading to the identification of the PI3K-Akt-ERK signaling pathway as a potential mechanism underlying HLB’s therapeutic effects in DN. The gene discussed is MAPK1; the disease is liver dysplastic nodule.