The results proved that RES protected NSCs from apoptosis, increased the proportions of NSCs in the S and G2/M phases, and significantly upregulated the expression levels of Nrf2, heme oxygenase 1 (HO-1), and NAD(P)H: quinone oxidoreductase 1 (NQO1) after ODG, indicating that RES is capable of positively regulating NSCs in stroke (Shen et al., 2016). The gene discussed is NFE2L2; the disease is stroke disorder.