Chk1 inhibition was found to exacerbate the effect of 5-FU by stimulating formation of H2AX foci and cytotoxicity, not only in wild type cells but also in HRR-deficient cells indicating that further understanding of how the ATR-Chk1 pathway impacts on 5-FU toxicity has implications for a range of cancers including those with APC mutations [29]. This evidence concerns the gene H2AX and cancer.