Excessive levels of ROS stress can exhaust the antioxidant capacity and promote apoptosis by increasing the ROS stress level beyond a threshold.28 Previous studies demonstrated that logical combinations of ROS-modulating compounds with chemotherapeutic drugs may further enhance therapeutic activity.29, 30 Recently, Yun et al.31 found that vitamin C–induced ROS inhibits GAPDH activity by NAD+ depletion, ultimately leading to cell death in BRAF and KRAS mutant CRC cells. The gene discussed is KRAS; the disease is colorectal carcinoma.