Indeed inhibition of Chk1 in tumor cells, either by siRNA knockdown of Chk1 protein expression [19], or by small molecules inhibiting its kinase activity, demonstrated its role in the potentiation of the cytotoxic activity of DNA damaging agents [18,19] This model is also supported by the findings that Chk1 inhibition preferentially sensitizes p53 deficient human cancer cells, but not p53 functional cells to gemcitabine, radiation and 5-fluorouracil [29,33,34]. Here, TP53 is linked to neoplasm.