One by one, mutation-containing mendelian genes that cause monogenic juvenile myoclonic epilepsies (JME) and single nucleotide polymorphisms (SNP)-susceptibility alleles that increase risks for nonmendelian complex JME should fall to the power of molecular genetics. Of 15 chromosome loci, 3 mendelian genes (alpha1-subunit of the GABA(A) receptor [GABRA1], chloride channel 2 gene [CLCN2], and Myoclonin1/EFHC1) and 2 SNP-susceptibility alleles of putative JME genes in epistases (bromodomain-containing protein 2 [BRD2] and connexin [Cx]-36) have been identified, so far. Antiepileptic drugs now can be designed against the specific molecular defects of JME.