IL1B and rheumatoid arthritis: Firstly, we modelled RA in vitro through stimulation of isolated primary rat chondrocytes with IL-1β—one of the key driving molecules in the majority of RA animal models [42,43]—in order to modify chondrocytes’ behavior and metabolism [44] and to promote oxidative stress [45,46], an event that contributes importantly to the pathogenesis of several human diseases, including RA [43,47].