NFKB1 and rheumatoid arthritis: After TL1A/DR3 binding, it can pathway synergistically promotes T cell activation, activates NF-κB pathway, induces apoptosis inhibitory proteins, thereby promoting the transcription and release of inflammatory factors TNF-α and IL-6, and participating in the regulation of immune response and the development of inflammatory diseases, include rheumatoid arthritis (RA), asthma, and autoimmune diseases (Aiba et al., 2014; Schmitt et al., 2024).