Prader–Willi syndrome (PWS) is a paternal structural abnormality involving 15q11-13, while a maternal aberration in the same region causes Angelman syndrome (AS). In both syndromes, the majority of cases (75%) are the result of a 3–5 Mb deletion of the PWS/AS critical region. These small aberrations cannot be detected using cytogenetics or conventional CGH, but can be readily detected using array CGH. As a proof of principle Vissers et al. (2003) constructed a genome wide array with a 1 Mb resolution to screen three patients with known, FISH-confirmed microdeletion syndromes, including one with PWS. In all three cases, the abnormalities, ranging from 1.5 to 2.9Mb, were readily identified. Thus, array CGH was demonstrated to be a specific and sensitive approach in detecting submicroscopic aberrations.