However, this doesnot explain the recessive transmission of the other hyperekplexia-causing mutations in GlyT211,12 or all known mutations in DAT, which give rise to childhood dystonia/parkinsonism8–10.The apparent oxymoron of having both, dominant and recessive SLC6 mutations, can be resolved by considering that oligomer formation occurs late in the folding trajectory. This evidence concerns the gene SLC6A3 and hyperekplexia.