In PC12 cells, glucose deficiency resulted in TFCP2 downregulating ASIC2a. On the other hand, hippocampal glucose hypometabolism, both in human patients with epilepsy and in rat epilepsy-model brains, increases ASIC2a expression by suppressing TFCP2 expression, which further enhances the intrinsic excitability of CA1 pyramidal neurons and escalates seizure susceptibility in patients with temporal lobe epilepsy [44]. This evidence concerns the gene ASIC2 and temporal lobe epilepsy.