Briefly, ATS is characterized by tortuosity and elongation of large- and medium-sized arteries and is caused by loss-of-function mutations in the SLC2A10 gene encoding the facilitative glucose transporter 10 (GLUT10), which facilitates the uptake of glucose and dehydroascorbic acid (DHA) [98,99]. This evidence concerns the gene SLC2A10 and Andersen-Tawil syndrome.