Its exact cause is unknown, but present research points toward a genetic and epigenetic component, possibly following maternal genes on chromosomes 7 and 11. It is estimated that approximately 50% of<unk><unk>  patients have hypomethylation of H19 and IGF2. This is thought to lead to low expression of IGF2 and over-expression of the H19 gene. In 10% of the cases the syndrome is associated with maternal uniparental disomy (UPD) on chromosome 7. This is an imprinting error where the person receives two copies of chromosome 7 from the mother (maternally inherited) rather than one from each parent. Other genetic causes such as duplications, deletions and chromosomal aberrations have also linked to<unk> . Interestingly,<unk><unk>  patients have variable hypomethylation levels in different body tissues, suggesting a mosaic pattern and a postzygotic epigenetic modification issue. This could explain the body asymmetry of the SRS phenotype. Like other imprinting disorders (e.g. Prader–Willi syndrome, Angelman syndrome, and Beckwith–Wiedemann syndrome),<unk>  may be associated with the use of assisted reproductive technologies such as in vitro fertilization.
Silver–Russell syndrome
Miller–Dieker syndrome
Meckel–Gruber syndrome
Laurence–Moon syndrome
Intestinal metabolic bromhidrosis syndrome
Miller syndrome
Nathalie syndrome
Halperin-Birk syndrome