Following NP exposure, the mitochondrial membrane potential was reduced and cytochrome C was released from the mitochondria to the cytoplasm; furthermore, an important anti-apoptotic protein (Bcl-2) was inhibited and initiated the activation of apoptosis-related proteins such as caspase 9 and 3, eventually aiding in the significant apoptosis of tumor cells. Here, BCL2 is linked to neoplasm.