Critical evaluation of this hypothesis will require functional studies similar to those described by Visser et al. [33], but it is interesting to note that the ∼1 Mb interval between HERC2 and APBA2 contains a cluster of segmental duplications that serves as a frequent deletion breakpoint (BP3) involved in Prader-Willi and Angelman syndromes [45]. This evidence concerns the gene APBA2 and Angelman syndrome.