SDRT induced in vivo and in vitro endothelial cell apoptosis via activation of ASMase/ceramide signaling, which contributes to tumor growth delay or cure [6, 9, 14]. Within these studies, SDRT triggered TEC apoptosis as early as 2 h and peaked at 6–8 h post radiation treatment [6, 14]. Our results showed that SDRT drove an increase of in vivo TEC and in vitro BAEC apoptosis at 6–8 h post RT, which supported these findings. Tumor vasculature has been shown to be largely affected by RT depending on the number of fractions, dose rate, and total radiation dose . SDRT can induce rapid apoptosis of TEC, whereas the importance of vascular damage in tumors receiving conventionally fractionated radiation therapy (CFRT: 1.8–2 Gy per fraction) is more controversial [6, 7, 30]. A recent study suggested that 2 Gy irradiation dose induced minimal endothelial cell apoptosis followed by a later increase in vessel diameter, microvascular density and vessel leakiness in normal brain blood vessels . However, few reports so far provided clear proof that CRFT induced TEC apoptosis. Thus, the biological mechanism underlying fractionated radiotherapy may greatly differ from SDRT used in this study, which mainly functions via ASMase/ceramide-mediated vascular dysfunction.