The fact that the downstream effector phosphoinositide-specific phospholipase C-γ1 (PLC-γ1) seems essential to BDNF/TrkB-mediated epileptogenesis in the kindling model [579] also points to BDNF/TrkB/PLCγ1 signaling as a possible molecular mechanism by which SE induces TLE [580,581] providing a new therapeutic target for possible epilepsy prevention. This evidence concerns the gene PLCG1 and epilepsy.