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When KCNB1 (a homolog of KVS-1) contacts with ROS, Src/JNK-meditated apoptotic program in mitochondria would be initiated to produce more ROS ( 2+ channel, would open more readily and thus, leak Ca 2+ after oxidation ( 2+ by activating inositol 1,4,5-trisphosphate receptors (IP3R) to open the permeability transition pore, thereby changing the permeability of mitochondria to further release more ROS as a vicious cycle (Sittl et al., 2012)

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