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). This evidence concerns the gene SLC2A1 and hyperinsulinemic hypoglycemia, familial, 4.