KCNMA1 and epilepsy: The mechanisms by which UBE3A LoF can lead to cortical hyperexcitability and epilepsy had long remained elusive, until recently one mechanism was suggested by the discovery that a lack of UBE3A‐mediated degradation of large conductance calcium‐activated potassium channels (BK) channels and resulting augmented BK channel activity leads to increased intrinsic cellular excitability (Sun et al., 2019).