Our identification of LNX1 and LNX2 as novel regulators of GlyT2 may have pathophysiological relevance on the biology of glycinergic neurotransmission and might help frame future investigations into the molecular basis of human disease states that are consequence of dysfunctional glycinergic neurotransmission, such as hyperekplexia and chronic pain. This evidence concerns the gene LNX1 and hyperekplexia.