A similar pattern was identified in NKX6‐2 with cases presenting clinically with spastic ataxia in the absence of hypomyelination and a reduction of NKX6‐2 protein levels (case F1‐III:1) compared to extended hypomyelination in cases with truncating mutations resulting in no expression of NKX6‐2 protein, as previously reported 2. This evidence concerns the gene NKX6-2 and spastic ataxia.