GPR65 and arthritic joint disease: Accordingly, the next step should be to look at the involvement of GPR65 in conditions with a higher degree of inflammation, which might also enable an assessment of how the endogenous acidosis associated with such conditions contributes to pathology, a starting point could be the antigen-induced arthritis model, which has been shown to cause joint acidosis in rats (4) and might offer a more translational assessment of the therapeutic potential of targeting GPR65.