Nonetheless, our results from the Cacna1iRH/RH mice linked a risk variant in schizophrenia with a quantifiable EEG endophenotype marker in NREM reported in schizophrenia patients, providing reverse and forward translational opportunities to understand deficits of sleep spindle and TRN function in schizophrenia6,9 and serving as a key step toward testing the therapeutic hypothesis that normalizing sleep spindles by targeting CaV3.3 and/or TRN function may lead to novel strategies for treating schizophrenia patients. The gene discussed is TNPO1; the disease is schizophrenia.