A large number of mechanisms have been proposed to explain the pathogenesis of post-stroke depression, including neuroinflammation, abnormal activation of the hypothalamic–pituitary–adrenal axis, abnormal expression of vascular endothelial growth factor, reduction of brain-derived neurotrophic factor, and dysfunction of monoamine neurotransmitters (MNTs).[16–18]. This evidence concerns the gene VEGFA and depressive disorder.