KCNH2 and schizophrenia: Besides its relevance in cardiac physiology, relative overexpression of a primate-specific, brain isoform of Kv11.1 (KCNH2–3.1), which lacks an N-terminal domain crucial for slow deactivation and therefore induces high-frequency, non-adaptive firing patterns in cultured cortical neurons, has recently been linked to an increased risk of schizophrenia ( Huffaker et al., 2009).