In the context of cerebral hypometabolism in this study, we have identified that DNA hypermethylation of GLUT1 (SLC2A1) and key glucose regulatory genes, including MTOR, BDNF, VEGFα, and MCT2 (SLC16A7), distinguishes FCDIIa/b from other FCD-subtypes (mMCD, MOGHE) and non-lesional in brain samples. The gene discussed is SLC2A1; the disease is fleck corneal dystrophy.