Among these, KD proved beneficial in metabolic epilepsies involving dysfunctional energy utilization (e.g., glucose transporter type 1 deficiency syndrome (GLUT1‐DS) and pyruvate dehydrogenase complex deficiency) or abnormal neurotransmitter degradation (succinic semialdehyde dehydrogenase deficiency and non‐ketotic hyperglycinemia), as well as in mitochondrial epilepsies (e.g., POLG‐related disorders and Leigh syndrome) (Gavrilovici & Rho, 2021; Lin Lin Lee et al., 2018). Here, ALDH5A1 is linked to metabolic epilepsy.