This might be due to the pure epithelial nature of MDA-MB-231 breast cancer cell types,[33] as it was verified that telomerase abrogation accelerates TRF2-induced epithelial carcinogenesis.[34] Furthermore, it has been illustrated that telomerase inhibition might not be effective to cease the growth of TRF2-overexpressing tumors.[34] Both TRF1 and TRF2 were reported as negative regulators of telomere length and their down-regulation was shown to be important to maintain telomeric DNA in cancer.[35] Therefore, their up-regulation might disturb the telomere dynamics. The gene discussed is TERF1; the disease is breast carcinoma.