below). The patient with the exon 3 mutation has an apparently mild form of this disorder, consistent with the disruption of only one of the two main Gsα variants, i.e. Gsα-L [34]. It is conceivable that, depending on the effector selectivity and relative expression levels of Gsα-L and Gsα-S in different tissues, this mutation impairs agonist responses in an effector- and tissue-specific manner. This possibility remains unexplored.
