Lin et al. (2015) studied the activity of EEHDW in a carcinogenic inflammatory environment and demonstrated that EEHDW treatment significantly reduced IL-6-induced STAT3 pathway phosphorylation and induced activation of pro-apoptotic factors Bax, caspase-9, and caspase-3, and downregulated Bcl-2, cyclin D1, and CDK4, thereby enhancing the local inflammatory environment and promoting tumor progression. Here, BCL2 is linked to neoplasm.