Additionally, LATS2 knockdown attenuated the alleviation of Rad51 and MDC1 nucleus accumulation induced by SFN, and then, to some extent, resumed the repair of DNA damage, indicating that LATS2 served as one of the downstream targets of SFN which inhibited Rad51 and MDC1 taking part in DSB repair and enhanced the radiosensitivity of cervical cancer cells. This evidence concerns the gene SFN and cervical carcinoma.