DNA damage caused by Pol β deficiency can activate the cGAS/STING/NF-κB signaling pathway, upregulate the expression of NLRP3, IL-1β, and IL-18, exacerbate macrophage pyroptosis and regulate the occurrence and development of RA, while Pol β overexpression downregulates inflammatory cytokines and impair macrophage pyroptosis. Here, IL1B is linked to rheumatoid arthritis.