There has been a single report of temporal lobe epilepsy associated with a mutation of the KV4.2 (Singh et al. 2006), but knockout studies have suggested that this produces a modest change in seizure threshold and cardiac investigations in the same mouse line showed that the phenotype is relatively benign with no overt cardiovascular pathology perhaps because of compensation from other potassium channel subunits (Guo et al. 2005). This evidence concerns the gene KCND2 and temporal lobe epilepsy.