Genetic mutations constitute the most popular etiology of SHE in the current literature, with identified SHE-related pathogenic genes including neuronal ligand-gated and ion-gated channel-related genes (CHRNA4, CHRNB2, CHRNA2, KCNT1, GABRG2), upstream genes in the mammalian target of rapamycin complex 1 (mTORC1) signaling pathway (DEPDC5, NPRL2, NPRL3, TSC1, TSC2), and other genes (CRH, CaBP4, STX1B, PRIMA1). This evidence concerns the gene GABRG2 and sleep-related hypermotor epilepsy.