IL23R and hereditary disease: B27 can explain no more than 30% of the overall genetic risks of AS.5 The mechanistic hypotheses of B27 causing AS are also not well established.6 Recently, two new loci related to AS, aminopeptidase regulator of TNFR1 shedding 1 (ARTS1) and the interleukin 23 receptor (IL23R), were independently reported in a North American cohort by 14 436 non-synonymous SNPs (nsSNPs) screen, confirming an AS related genetic disorder outside HLA-B27 through case–control association study.7