Pro-inflammatory mediators, such as tumour necrosis factor-α (TNF-α), interleukin (IL)-1, IL-6 and matrix metalloproteinases (MMPs) play a significant role in promoting inflammatory infiltration, synovial hyperplasia, joint destruction, and various comorbidities associated with RA (Zhai et al., 2017; Guo et al., 2018). This evidence concerns the gene IL1B and rheumatoid arthritis.