NO inhibits apoptosis by blocking caspase activity, increasing Bcl‐2 expression, inducing heat‐shock proteins HSP70 and HSP32, suppressing the release of cytochrome C, and decreasing cyclooxygenase‐2 activation.[138] NO also promotes arteriolar dilation which increases blood flow to the tumor, thereby inducing the angiogenesis necessary for tumor progression. This evidence concerns the gene BCL2 and neoplasm.