<unk>  results from mutations in the MLL (also known as KMT2A) gene on the long arm of chromosome 11. The gene encodes a histone-modification enzyme — that is, it helps modify the expression of other genes. The condition is autosomal dominant, meaning that only one abnormal copy of the gene is needed for a person to have the syndrome. In a majority of cases to date, the mutation occurred de novo — that is, neither parent was affected and the mutation is sporadic. Offspring of those with WSS have a 50% chance of having WSS. The mechanism by which mutations in the MLL gene cause the phenotype of<unk>  is not yet known.
Wiedemann–Steiner syndrome
Beckwith–Wiedemann syndrome
Wiedemann–Rautenstrauch syndrome
Laurence–Moon syndrome
Bardet–Biedl syndrome
Wilson–Turner syndrome
Miller–Dieker syndrome
Smith–Magenis syndrome