The syntenic area on human chromosome 14 is the critical region for Temple Syndrome, and loss of DLK1 expression is thought to cause phenotypes associated with this disorder; pre-and postnatal growth restriction with increased truncal obesity and precocious puberty (Ioannides et al., 2014). This evidence concerns the gene DLK1 and motor developmental delay due to 14q32.2 paternally expressed gene defect.