While the present and other studies suggest that prolonged treatment with TGFβ1 or a downstream effector of the TGFβ1/ALK5 signaling pathway may be used to enhance plasticity and extend its critical window after stroke (Li et al., 2015; Zhang et al., 2019), a systemic delivery of TGFβ1 would bring about unwanted negative side-effects owing to the plethora of functions of TGFβ1 as a inflammation related molecule (Akhurst and Hata, 2012). This evidence concerns the gene TGFB1 and stroke disorder.