Lack of these important connections apparently makes as a competitive inhibitor, that will be in line with above findings SCR7. f SCR7 o-n homologous recombination and NHEJ, an HR deficient cell line, HCC1937 was used. Results showed improved awareness of the cell line to SCR7, compared to its wild type, MCF7, showing that in the absence of HR, DSBs generated due to obstruction of Ligase I-V remain ubiquitin conjugating unrepaired leading to increased cell death. To further examine whether the cytotoxicity observed was particular to Ligase IV inhibition, N114, and Nalm6 cells were treated with increasing levels of SCR7. Results confirmed that N114 remained unresponsive to SCR7, while Nalm6 demonstrated a dose-dependent increase in cytotoxicity. To ensure the statement, we knocked down Ligase I-V by utilizing antisense plasmid in MCF7, Nalm6 and HeLa cells. Treatment of the cells with SCR7 led to the increasing loss of sensitivity, compared to sensitivity of mock transfected wild type cells, establishing its nature to Ligase IV. Likewise, overexpression of Ligase Eumycetoma IV led to relief of these cells from SCR7. Besides, knock-down of Ligase III in Nalm6 didn’t bring about significant loss in cytotoxicity, suggesting that SCR7 exerts its effects by targeting Ligase IV. It has been proven that blocking NHEJ can rescue interstrand crosslink re-pair defects in Fanconi Anemia deficient cells. We reasoned that SCR7, being a NHEJ chemical, might curb ICL awareness in FANCD2 deficient cells. To try this, we treated human PD20 cells with mitomycin C and SCR7. Results showed that therapy of MMC in PD20 led to increased awareness. Curiously, improvement of MMC along with SCR7 displayed higher-level of emergency indicating that SCR7 could block NHEJ in FANCD2 deficient cells. Elevated levels of chromosomal aberrations including deletions were also seen in HeLa cells upon treatment with SCR7. We tested different mice models, to assess the effect of SCR7 on cyst development. Results showed that SCR7 therapy considerably reduced breast adenocarcinomainduced tumor. Untreated growth animals survived only for 52 days, whereas treated animals displayed 4 fold increase in lifespan. We also tested the efficiency of SCR7 o-n Daltons lymphoma mouse model and found neither cancer regression or escalation in life. Gross appearance of thigh tissues, liver, and spleen of treated and control animals about the 25th and 45th day after tumor development showed effect of SCR7 in-a time-dependent fashion. Histopathological evaluation showed tumor cell growth in tumor settings, while a decrease was apparent upon SCR7 treatment. Morphology of hepatocytes within the treated group was similar to that of normal animals.