Support for this theory with respect to IBD-SpA includes specific patterns of gut dysbiosis seen in patients with SpA [11] as well as a number of shared genetic risk loci, including interleukin (IL)-23R for IBD and ankylosing spondylitis and nucleotide-binding oligomerization domain (NOD)2 for IBD and sacroiliitis [9, 12]. Here, NOD2 is linked to inflammatory bowel disease.