Research on the pathophysiology of depression have not only indicated significant upregulation of the N-methyl-D-aspartate receptor- (NMDAR-) dependent calcium/calmodulin-dependent protein kinase II beta (β-CaMKII or CaMK2B) in the lateral habenular nucleus of the central nervous system of depressive-like animal models but also shown that some antidepressants could reduce the level of CaMK2B in the hippocampus [11]. This evidence concerns the gene CAMK2B and major depressive disorder.