A classic example of this phenomenon are SNPs in the mouse SCNM1 gene, a splicing regulator of the neuronal sodium channel gene Scn8a, whose SNP-related splicing variant can convert mild-movement disorders into paralysis by simply shifting the splicing pattern of its target gene Scn8a, which is also sensitive to SNP-related alternative splicing of its own sequence89. This evidence concerns the gene SCN8A and movement disorder.