Secondly, molecular disruptions affecting the 11p15.5 chromosomal imprinting genes associated with BWS also play a significant role.[17] Approximately 25% of PMD cases reportedly co-occur with BWS.[18] Features of BWS include loss of methylation of DMR2, hypermethylation of DMR1 on the maternal allele, mutations in the maternal CDKN1C gene, and biallelic expression of normally paternally imprinted genes. The gene discussed is CDKN1C; the disease is Pelizeaus-Merzbacher spectrum disorder.