Previous work on stroke models has shown that EphA4 activation exacerbates brain edema and reduces functional recovery,[21] while inhibiting EphA4 could confer neuroprotection and enhance collateral response.[11] Furthermore, the use of Tie2‐Fc in EphA4 KO mice to block Tie2 signaling attenuated their response back to WT levels, further supporting crosstalk between EphA4 and Tie2.[11]. The gene discussed is EPHA4; the disease is stroke disorder.