We identified three NIPA2 mutations (c.532A > T, c.731A > G, c.1002_1003insGAT) from children with CAE.10, 11 However, we did not find NIPA2 variations in children with epilepsy and intellectual/developmental disabilities through targeted next‐generation sequencing or Sanger sequencing.45 A subsequent functional study has verified that these three mutations are loss of function.12 In the present study, the dysfunction of NIPA2 enhanced the excitability of neocortical somatosensory pyramidal neurons by decreasing BK channel currents. Here, KCNMA1 is linked to epilepsy.