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. Here, H2AX is linked to lung carcinoma.