Abdoulaye et al found that the expression of β-CaMKII was significantly increased after Chlorimipramine treatment in an animal model of stroke-induced depression.[34] He et al found that activation of CaMKII expression in neurons can alleviate cognitive dysfunction induced by inflammation in an inflammatory model.[35] Zhang et al confirmed that activation of the CaMKII-related signaling pathway can improve depression-like behavior in rats by enhancing synaptic plasticity.[36] These study results suggest that CaMKII may be involved in the development of depression. Here, CAMK2G is linked to stroke disorder.