Further, evidence that the hedgehog pathway is downstream of the androgen receptor is supported by findings that Gli2 and Gli3 mutant mouse models, in addition to temporally controlled deletion of Shh between E13.5 and E15.5, cause hypospadias and a urethral phenotype that is strikingly similar to the hypospadias observed in Gli3XtJ mutants [10,11,52]. This evidence concerns the gene SHH and hypospadias.