Interestingly, studies that aimed to link the extent of β2 microglobulin misfolding to UPR activation, inflammation, and SpA development in HLA B27-transgenic rats demonstrated that the introduction of additional copies of the human β2-microglobulin gene, which reduced HLA-B*27 misfolding and UPR activation, led to an increase in the incidence and severity of arthritis [55], rather than the expected decrease. The gene discussed is HLA-G; the disease is Arthritis.