The loss of GBX2 function also modulates the Slit/Robo-signaling pathway, leading to abnormal NCC migration and abnormalities that as similar to those in congenital diseases, such as DiGeorge syndrome and in craniofacial malformations (Byrd and Meyers, 2005; Calmont et al., 2009). This evidence concerns the gene GBX2 and 22q11.2 deletion syndrome.