This suggests a role for R-spondins in facilitating epithelial repair as a response to mucosal injury, which is consistent with enhancement of Wnt signaling during intestinal regeneration [28] and with the observations that genetic reduction or pharmacological inhibition of Dkk1 during DSS colitis has been shown to promote wound repair by increasing proliferation of epithelial cells [37]. Here, RSPO1 is linked to colitis.