It has been proposed that the phenotypic variability in Gas1 and Cdon mutant mice, which display a range of holoprosencephaly phenotypes, might be partially caused by the stochastic changes in establishment and response to the SHH morphogen gradient in a complex developmental program, where Shh is expressed in a temporal sequence as neural tissues develop with additional differences in the expression of multiple HH receptors also contributing to variability in holoprosencephaly severity [15]. This evidence concerns the gene CDON and holoprosencephaly.