In some patients, the complexity of the clinical phenotype could be partially related to the extension of microdeletions on chromosome 19 leading to haploinsufficiency of a variable number of genes contiguous to KMT2B. Notably, a marked improvement of dystonia with sustained clinical benefit on long-term follow-up has been reported following bilateral GPi DBS, whereas no oral medication is reported to be particularly effective in alleviating motor manifestations [26••, 27••, 28]. Here, KMT2B is linked to Dystonia.