The GOF property of WAG-HCN1 (animal model of absence seizures) is caused by N-terminal deletion, change in N-terminal wild-type sequence (GNSVCF) motif, increased current, enhanced HCN1 expression, reduced cAMP sensitivity, and suppressed HCN2 and HCN4 currents according to the functional analysis performed on Xenopus oocytes and thalamus of WAG/Rij rat strain (Wemhöner et al., 2015). The gene discussed is HCN2; the disease is juvenile absence epilepsy.