IL1B and rheumatoid arthritis: A number of inflammation stimuli, including TNF-α, IL-1β, IL-6, or ROS, can activate proinflammatory pathways involved in RA pathogenesis, concerning predominantly nuclear factor-κB (NF-κB), mitogen activated protein kinases (MAPKs), or Janus kinases/signal transducers and activators of transcription (JAK/STAT1/3) [6–8].