In addition, we have demonstrated that VAV2 overexpression may cause the activation of STAT1 signaling in response to IR and inhibition of STAT1 activity by Fludarabine significantly reverses the vulnerability of ESCC cells to IR in vitro and in vivo in mouse xenograft models, suggesting that the VAV2-STAT1 axis is a target for improving radiotherapy. The gene discussed is STAT1; the disease is esophageal squamous cell carcinoma.