addition of SCR7, a decrease in the recombination, subsequent normalization of transfection efficiency, was observed indicating inhibition of NHEJ in the intracellular level. Centered on the above observations, we wondered whether the inhibition of implicit NHEJ could result in the accumulation of unrepaired DSBs at the level. To check this, breast and cervical GW0742 cancer cell lines were treated by us with SCR7, followed by immunofluorescence and western blotting studies, by using anti gH2AX. Results showed a growth in quantities of gH2AX foci and protein, indicative of unrepaired DSBs with-in cells. How many foci observed on account of SCR7 was similar to those developed during siRNA knock-down of Ligase IV. As a control, we employed scrambled siRNA and siRNA against Ligase I and III. But, similar tests o-n K562 cells didn’t provide any gH2AX foci, also at highest concentrations of SCR7, perhaps Infectious causes of cancer as a result of low expression of Ligase I-V. In-dependent of N114, Ligase IV, and Nalm6 cells were treated with SCR7 and examined for gH2AX amounts by immunofluorescence and western blotting, to exclude the possibility that SCR7 can create DSBs immediately. Results showed that gH2AX expression remained unchanged upon SCR7 therapy in Ligase IV / cells, although a substantial increase was observed in case of Nalm6 cells. Both the cell lines showed large advancement in gH2AX and foci appearance upon bleomycin treatment, a known DSB causing agent. Overall, these results claim that SCR7 doesn’t cause DSBs straight to the genome and is Ligase IV dependent. Besides, upon incubation of oligomeric dsDNA or supercoiled plasmid DNA with increasing levels of SCR7, there clearly was no evidence for DNA breaks. Thus, SCR7 inhibits NHEJ in cells, ultimately causing accumulation of unrepaired DSBs. To evaluate whether accumulation of DSBs leads to cell death upon SCR7 therapy, we conducted a comparison of cytotoxicity among various human ALK inhibitor cell lines derived from breast, cervical, lung, and ovarian cancers, fibrosarcoma, and leukemia, through the use of either MTT or trypan blue exclusion assays. Results showed a dose-dependent decrease in cell proliferation of MCF7, A549, and HeLa using an IC50 of 44 mM, respectively, that has been further confirmed by DIC imaging in MCF7. T47D, A2780, and HT1080 were also painful and sensitive to SCR7, with an IC50 of 1-0 mM, respectively. On the other hand, SCR7mediated cytotoxicity was confined when leukemic cell lines were used, with the exception of Nalm6, which confirmed an IC50 of 50 mM. Appearance of Ligase IV in various cancer cells could be linked with their sensitivity to SCR7, with an exception of T47D, that has low quantities of Ligase IV. This might be perhaps as a result of change in the proapoptotic to antiapoptotic rate, because of its aberrant BCL2 position. To determine the result o