KCTD17 and myelodysplastic syndrome: KCTD17 (c.434G > A, p.Arg145His) was the only segregating variant among seven candidates from affected myoclonus‐dystonia patients in the British family.79 Very recently, two additional KCTD17 mutations affecting the same splice acceptor site (c.508‐2A > T and c.508‐1G > T) were identified in two independent studies.81, 82 It has been pointed out that the clinical features of the KCTD17 patients are phenotypically distinguishable from MDS due to SGCE mutations.80 However, the evidence is reasonably compelling that KCTD17 mutations are responsible for a subset of myoclonus‐dystonia.