Increased fatty acid oxidation, either as a direct cause of the disease or a consequence of down-regulation of GLUT3 or glucose intolerance in ALS patients [43], may lead to reduced fat storage which is observed in ALS patients as disease progresses [45,46] and could lead to dyslipidemia which is a prognostic factor in the disease [47]. Here, SLC2A3 is linked to amyotrophic lateral sclerosis.