CUL4B and X-linked intellectual disability: The disruption of CUL4B in the epiblast, but not in extra-embryonic tissues, allows CUL4B-deficient embryos to survive, and the resulting viable mice display defects in spatial learning and memory, which are consistent with the fact that CUL4B loss-of-function mutations are frequently associated with X-linked intellectual disability in humans [54,55,56].