KEGG and GO enrichment linked the polyphenol-modulated target set to cytokine–cytokine receptor interaction, JAK–STAT, NF-κB, IL-17, TNF, RA, and arachidonic-acid pathways (Supplementary Table 3), as well as biological processes including inflammatory response, extracellular matrix degradation, and nitric-oxide biosynthesis (Supplementary Table 3), confirming that the ligand panel collectively covers the critical effector axes of RA pathogenesis, Fig. 3(c). This evidence concerns the gene NFKB1 and rheumatoid arthritis.