This hypothesis may be supported by the observation that 5-HT2A receptors are widely distributed and expressed in neuronal cell somata and dendrites of the DCN, and 5-HT could regulate the release of many neurotransmitters such as glutamate and GABA in cerebellum [27, 28], but the exact relationship between DCN activation and 5-HT2A receptor-mediated signaling in the EE-induced post-stroke recovery needs further exploration. This evidence concerns the gene DCN and stroke disorder.