The interaction between DAPK1 and GluN2B in the medial prefrontal cortex was recently found to contribute to the development of depressive-like behavior [16,17], and several studies have confirmed that DAPK1 is a promising target for the treatment of strokes, especially to prevent neuronal apoptosis in neuronal cell death [18,19,20]. Here, DAPK1 is linked to stroke disorder.