While both neurogenic and myogenic factors would contribute to the observed GI symptoms, the lack of clinical evidence for ANS and ENS dysfunction in DM-associated GI dysmotility in combination with the overall higher expression of DMPK and CNBP in SMCs (Genotype-Tissue Expression Portal [GTEx]) suggests that prominent GI phenotypes most likely arise from some aspect of smooth muscle dysfunction. This evidence concerns the gene DMPK and Gastrointestinal dysmotility.