In accordance with our results, PP2A has been suggested to participate in cranial morphogenesis through the regulation of cranial neural crest cell migration [55], and increased PP2A activity has been implicated in the pathogenesis of the Opitz Syndrome [31], [32], a complex congenital disorder characterised i.a. by brain and midfacial defects such as cleft lip and palate [56]. This evidence concerns the gene PTPA and Opitz G/BBB syndrome.