KCTD17 and Myoclonus: KCTD17 has also been reported to function as an adaptor of the cullin‐3 ubiquitin ligase to mediate ubiquitination and degradation of trichoplein, which is a negative regulator of ciliogenesis.32 Both neurons and astrocytes contain a primary cilium, and ciliogenesis has been reported to play an important role in brain development.84 This raises the possibility that defective ciliogenesis caused by KCTD17 mutations contributes to the pathology of myoclonus‐dystonia.