In conclusion, we present evidence that the Nrg1 TM HET mouse is not a traditional gene ‘knock-out’ model of Nrg1 haploinsufficiency, and we suggest that our findings are consistent with a gain of function model, aligned with the finding of increased NRG1 in the brains of human patients with schizophrenia [6]. This evidence concerns the gene NRG1 and schizophrenia.