While in DRE it remains currently unclear how the cKD works despite a much better understanding of anticonvulsant mechanisms [4], in the GLUT1-DS and PDCD it is the treatment of choice in order to switch brain metabolism from glucose to ketone bodies (KBs) and leading to a powerful improvement in neurologic symptoms. The gene discussed is SLC2A1; the disease is pre-descemet corneal dystrophy.