We used four approaches to demonstrate that tumor cells deficient in the FA pathway are hypersensitive to CHK1 inhibition: 1) siRNA knockdown of FA genes 2) FA gene mutant and corrected isogenic lines; 3) a morpholino knockdown of FANCD2 in a zebrafish model; and 4) pharmacologic inhibition using two CHK1 inhibitors, Gö6976 and UCN-01. This evidence concerns the gene FANCD2 and neoplasm.