In this study, we demonstrated that activation of HIF-1 by genetic or pharmacological means induced metabolic reprogramming and attenuated the ROS generation and cell death induced by a clinical relevant concentration of propofol; these effects were observed in both the established renal carcinoma RCC4 cell line and in the neuroblastoma SH-SY5Y cell line. Here, HIF1A is linked to renal carcinoma.