Therefore, molecular docking indicates that the compound can bind RELA (p65) and TNFRSF1A with relatively favorable scores (both < −5.90), consistent with the potential to interfere with NF-κB and TNF–α signaling pathways and the activity or localization of the p65 subunit of NF-κB mechanisms that are highly relevant to rheumatoid arthritis pathogenesis [33]. Here, NFKB1 is linked to rheumatoid arthritis.