Because UA blocks VRK1 kinase activity, we predicted that treatment with this molecule would also lead to elevated γ-H2A.X, and as expected, we found that UA treatment induces γ-H2A.X in lung cancer cells (Fig. 3c,d), suggesting that UA leads to the accumulation of DNA damage by blocking the kinase activity of VRK1. This evidence concerns the gene H2AX and lung cancer.