The amount of TNF-α produced by B cells in RA patients increases after the activation of Toll-like receptor 9 (TLR9) and CD40, which ultimately increases the expression of the receptor activator of the nuclear kappa beta ligand (RANKL) in the presence of IL-1β and promotes the formation of osteoclasts (Yeo et al., 2015). Here, IL1B is linked to rheumatoid arthritis.