Tyagi et al. [7] studied the mitochondrial mechanism of microvascular endothelial cell apoptosis caused by hyperhomocysteinemia and found that HCY-mediated ROS production promotes endothelial cell apoptosis in part by disturbing MP (decrease and loss of MP), which results in subsequent release of cytochrome-c and activation of caspase-9 and caspase-3, leading to cell death. This evidence concerns the gene CYCS and hyperhomocysteinemia.