It mainly occurs due to mutations in the solute carrier family 2 member 1 (SLC2A1) gene, resulting in the reduced or partial loss of GLUT1 expression; thus, glucose cannot effectively pass through the BBB, leading to neuronal energy deficiency, impaired brain function, and finally, to a series of neurological symptoms (6). This evidence concerns the gene SLC2A1 and hyperinsulinemic hypoglycemia, familial, 4.