DNA repair mechanisms are essential for cellular survival in mammals. A rapid 
repair of DNA breaks ensures faster growth of normal cells as well as cancer 
cells, making DNA repair machinery, a potential therapeutic target. Although 
efficiency of these repair processes substantially decrease the efficacy of 
cancer chemotherapies that target DNA, compromised DNA repair contributes to 
mutagenesis and genomic instability leading to carcinogenesis. Thus, an ideal 
target in DNA repair mechanisms would be one that specifically kills the rapidly 
dividing cancer cells without further mutagenesis and does not affect normal 
cells. Endo-exonucleases play a pivotal role in nucleolytic processing of DNA 
ends in different DNA repair mechanisms especially in homologous recombination 
repair (HRR) which mainly repairs damaged DNA in S and G2 phases of the cell 
cycle in rapidly dividing cells. HRR machinery has also been implicated in cell 
signaling and regulatory functions in response to DNA damage that is essential 
for cell viability in mammalian cells where as the predominant nonhomologous 
end-joining pathway is constitutive. Although HRR is thought to be involved at 
other stages of the cell cycle, it is predominant in growing phases (S and G2) 
of the cell cycle. The faster growing cells are believed to carryout more HRR in 
replicative stages of the cell cycle where homologous DNA is available for HRR. 
Targeting endo-exonucleases specifically involved in HRR will make the normal 
cells less prone to mutagenesis, rendering the fast growing tumor cells more 
susceptible to DNA-damaging agents, used in cancer chemotherapy.