The observed significant elevation of AT1R and reduced MasR/AT1R (Figure 6) support the notion that arthritis can change the vasodilation–vasoconstriction balance as there will be less target protein, MasR, for coupling with already reduced vasodilator Ang-(1-7), and, on the other hand, more AT1R is available to be activated by a higher concentration of a vasoconstrictor, Ang II. This evidence concerns the gene ANG and arthritic joint disease.