Analysis of copy number variation on chromosome 21 may, therefore, lead to a better understanding of the etiology of DS sub-phenotypes and could possibly shed light on the origin of these conditions in the wider non-trisomic population. Knowledge of which genes are involved in the generation of CHD in DS, for example, and how they interact with other gene products, could have many implications for managing CHD in the non-trisomic population: for example, adult onset CHD may be prevented by therapeutic agents that target critical pathways controlling cardiogenesis, and new approaches may be developed for stem-cell guided cardiac repair (reviewed in Passier et al. 2008) .