The four non-imprinted and biallelically expressed genes, NIPA1, NIPA2, CFYIP1 and TUBGCP5, in this microdeletion were initially noted to impact the severity of clinical presentation and neurological impairment in these two classical genomic imprinting disorders, Prader–Willi and Angelman syndromes with typical 15q11–q13 deletions depending on the absence or presence of the genomic area between breakpoints BP1 and BP2 containing these four genes, which led to the recognition of this microdeletion (Burnside–Butler) syndrome [4]. This evidence concerns the gene TUBGCP5 and Angelman syndrome.