The prolonged antitumor effects of BEZ235 maintenance treatment in CRC cell lines and HCT116 xenograft tumor tissue are mainly attributed to the continuous downregulation of molecules related to mTOR signaling (rpS6 and eIF4E) and the DNA-DSB repair pathway (ATM and DNA-PKcs) resulting from concurrent BEZ235 and RT treatment. The gene discussed is PRKDC; the disease is colorectal carcinoma.