This leads to impaired glucose transport into the brain and RBCs,11 manifesting as a range of neurological symptoms, including epilepsy, developmental delay, and movement disorders.12, 13, 14 The neurological disease can be modeled in mice by introducing heterozygous GLUT1 mutations,15 but because GLUT1 is only expressed in erythrocytes during the murine perinatal period and is rapidly replaced by GLUT4 in adult mouse erythrocytes, the impact of haploinsufficiency of GLUT1 on RBCs cannot be fully modeled in mice. This evidence concerns the gene SLC2A1 and movement disorder.