Given that heterozygous LGI1 mutations underlie ADLTE, previous studies have attempted to identify dominantly inherited mutations in ADAM22 in ADLTE families.37,38 However, the fact that the parents of the proband—who are heterozygous carriers of loss-of-function mutations—do not have epilepsy indicates that heterozygous deleterious mutations are tolerated in ADAM22 and that ADAM22 is primarily a recessive disease gene. This evidence concerns the gene ADAM22 and epilepsy.