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). The gene discussed is UBE3A; the disease is epilepsy.