Looking at the results of Rösler et al., who detected an induction of TFF3 gene expression due to stimulation of cultivated primary chondrocytes with TNFα and IL-1β [19], and considering the fact that TNFα and IL-1β are well known as important mediators of inflammation [47,48] it seems possible that this mechanism is the reason for the significantly higher level of TFF3 in RA synovial fluid. Here, IL1B is linked to rheumatoid arthritis.