Following individual-nucleotide resolution UV crosslinking and immunoprecipitation (iCLIP) experiments, all the PWS SPAs and sno-lncRNAs were shown to interact with various splicing factors including TDP43, RBFOX2 and hnRNP M. Through the sequestration of up to 1% of the total cellular level of these proteins, SPAs were found to regulate several splicing events in genes involved in synaptogenesis, hinting at a relationship between the aetiology of PWS and the dysregulation of splicing factor localization. Here, SLU7 is linked to Prader-Willi syndrome.