of NC cells migrating to their destinations might be a result of (1) a defect in the EMT, (2) an inability of NC cells to adhere to fibronectin, and (3) cell death as a consequence of anchorage loss of NC cells. Thus, our study suggests that MCEDS might add to the list of neurocristopathies. The identification of NC cells as a target of DS deficiency might help explain the other clinical criteria of MCEDS (Kosho, 2016). For example, it remains to be investigated whether the congenital heart defects in patients could be caused by an insufficient contribution of NC cells to the cardiac septum and valve formation, and whether recurrent subcutaneous infections in patients might reflect a compromised immune defense as a result of a reduced ability of NC cells to contribute to the thymus. In view of the multitude of cell types and tissues that NC cells give rise to (Le Douarin and Dupin, 2012), additional, new manifestations, e.g. in inner organs, might be identified that improve the diagnosis and etiology-based therapy of this currently intractable disorder.
