The fact that, in cells from HDs, folded B27 molecules exhibited similar turnover to those of other B alleles constrains mechanistic models of B27 misfolding, a factor thought to contribute to various mechanisms linking this allotype to genetic risk of spondyloarthritis in transgenic rodent models [59, 60] and in humans [61–63]. The gene discussed is MRAP; the disease is spondyloarthropathy.