HCN1 and epilepsy: If the hypothesis from Fan et al. [50] about increased membrane expression of HCN1 in pyramidal neurons being a kind of negative feedback in response to increased excitatory input to maintain network stability turns out to be correct, it is possible that the decreased HCN1 and Ih current of CA1 pyramidal cells in epilepsy refers to the failed compensation to increased excitatory inputs, and increasing HCN1 or Ih current may have value as therapeutic targets for epilepsy.