Nevertheless, owing to different tissue distributions, AGC2 mutations cause citrin deficiency, affecting primarily the liver, whereas AGC1 mutations lead to AGC1 deficiency and defective myelin synthesis, associated with hypotonia, arrested psychomotor development, seizures, spasticity, epilepsy, hypomyelination, and cerebral atrophy [33,34]. Here, SLC25A13 is linked to Cerebral atrophy.