Interestingly, using a mouse model of Prader-Willi syndrome, Stefan et al. (2005) [25] found that loss of expression of the MAGEL2 region induces upregulation of SH3RF2 and its flanking genes TCERG1, LARS, RBM27 and GPR151. As both the MAGEL2 and the SH3RF2 regions were flagged in the present study, a trans-acting regulatory mechanism involving the loci on chromosomes 7 and 21 found here is likely to underlie SC variation. This evidence concerns the gene RBM27 and Prader-Willi syndrome.