SHH and Pallister-Hall syndrome: A mouse model for PHS has been generated which exhibits most of the characteristic phenotypes (Böse et al., 2002); however, no pituitary defect has been identified in this mutant, suggesting that GLI3R activity during mouse pituitary development may be compensated, and that phenotypes we observe in Fuz−/− mice are more likely to be associated with an overall decrease in response to Shh than an increase in GLI3R‐mediated repression.