In each case, differential expression was apparently not due to alternative splicing, but reflected the use of alternative transcription start sites (OLFM1, MYO15A, NRXN1, IQSEC1, NAV1, and GSE1) or alternative termination sites (LAMP2, GNAO1 and HERC2P3 pseudogene–a frequent breakpoint in PWS patients) (Fig. S8B). Here, HERC2P3 is linked to Prader-Willi syndrome.