Multiple lines of evidence have increasingly suggested a pathogenic connection between the RA process and the mechanisms of T2D in a vicious circle perpetuated by glucose derangement and inflammatory mediators.

Some clinical studies showed that the inhibition of inflammatory cytokines, mostly IL-1, may allow the treatment of RA and concomitant T2D at the same time.

The presence of T2D may allow the physicians to perform a better profile of patients with RA according to the principles of precision medicine, tailoring the medical treatment to the individual characteristics.