Purpose of review: The spectrum of spondyloarthritis is characterized by the intriguing co-occurrence of gut and joint inflammation, although no obvious anatomical link exists. Recent findings: Data from animal models identify stromal cells as important players in pathogenesis, although signalling through TNFRI appeared to be sufficient for development of combined gut and joint inflammation. Interleukin-23 receptor was identified as a susceptibility locus for ankylosing spondylitis. Summary: Human genome studies combined with animal model research provide us with new evidence in the fascinating field of the gut-joint axis. However, how these newly identified genetic associations can influence the immunological environment remains to be elucidated.