Existing research has shown that the reduction or mutation of SLC25A32 may induce multiple acyl-CoA dehydrogenase deficiency, human myelomeningocele, MADD and related deficiencies, riboflavin-responsive exercise intolerance, neural tube defects and other diseases [22, 33–35]. This evidence concerns the gene SLC25A32 and multiple acyl-CoA dehydrogenase deficiency.