An early study showed TRIP-Br1 knockout mice displayed no overt pathology, except for certain abnormalities in pancreatic islets, including a reduction in the number of islets and the area of beta-cells, impaired insulin secretion, and glucose intolerance; these presumably resulted from the loss of TRIP-Br1’s regulatory function in cell cycle (Fernandez-Marcos et al., 2010). Here, CXCL11 is linked to Glucose intolerance.