The deletion of chromosome 15q11-q13, which encompasses MKRN3, contributes to the Prader–Willi syndrome, but it is not yet known which specific genes in this region are related to the syndrome.38 Analyses of balanced translocations in patients with the Prader–Willi syndrome have implicated the SNURF–SNRPN locus, which is telomeric to MKRN3. One report described 2 patients with all the features of the Prader–Willi syndrome who did not have a deletion of MKRN3, suggesting that MKRN3 deletion is not necessary to cause the syndrome.38 This report also described a patient with a paternal deletion of MKRN3, MAGEL2, and NDN who had only a few features of the Prader–Willi syndrome: obesity, developmental delay, and a high pain threshold. This patient also had signs of puberty at the age of 7 years 6 months, with advanced bone age. The patient received a diagnosis of central precocious puberty, which was supported by her response to treatment with triptorelin.38 Given our data, the deletion of MKRN3 is probably the cause of early puberty in this patient.38 It is uncertain whether the obesity, developmental delay, and high
