For example, GR physically interacts with CRY1/2 in a GC-induced manner and, in the post-prandial phase, CRY1/2 represses GR activity on e.g. the expression of Pck1. CRY1/2 deficient mice have constitutively high GC levels and exhibit glucose intolerance, suggesting reduced suppression of HPA axis and increased GR activity in the liver (99). This evidence concerns the gene NR3C1 and Glucose intolerance.