Interestingly, the paralogous genes ANO3 and ANO5 that encode putative Ca2+‐activated Cl‐ channels are mutated in autosomal dominant craniocervical dystonia (DYT23) and LGMD type 2L, respectively.61, 62, 63 Taken together, these data may suggest that abnormal Ca2+ signaling may play a broader role in the molecular pathogenesis of dystonia than previously thought.64 Our data also suggest that restoration of the complete SGC in cell models of M‐D, including patient‐derived induced pluriopotent stem cells, may be a useful translational biomarker for preclinical studies on M‐D. The gene discussed is ANO5; the disease is dystonia 23.