PACSIN1 and hereditary hyperekplexia: Given the multiple effects of the GlyR α1P366L mutation, and the different behavior of the GlyR α1P366L mutation in peptide arrays, immunoprecipitation, and label‐free quantitative MS/MS assays, it is not possible to state with certainty that disrupted GlyR α1‐syndapin I interactions are the cause of startle disease in this case.