Heterozygous deletion of GLUT3 correlates directly with expression levels of GLUT3 and influences glycolysis rates in the human immune system (46), but the frequency of the GLUT3 copy number variant is not different among RA, multiple sclerosis and heathy control, providing no evidence for RA protection in deletion of GLUT3 (46), the study of which demonstrated GLUT3 is not necessary for glucose transfer in patients with RA. Here, SLC2A3 is linked to multiple sclerosis.