In contrast to the depressive-like phenotypes reported after SCN or overall cortex KO20,54,56, the CaMK2a-Bmal1KO mice exhibited both stress-resilient and antidepressant-resistant behavioral changes, suggesting that Bmal1 expression and clock function in these particular neurons in mPFC may be an important factor in vulnerability to stress and the development and treatment of depression-like behavior12. This evidence concerns the gene CAMK2A and depressive symptom measurement.