This has been outlined in several in vitro and in vivo studies through the downregulation of Bcl-xL and FAP-1 expression, enhancing ROS generation, phosphorylating BAD and Bcl-2, upregulating caspase-3,8,9 activities, blocking cells at G0/G1 cell cycle phase, overcoming cancer cell resistance by inhibiting several ABC transporters through cGMP elevation, and increasing autophagosome and autolysosome levels; inducing tumor cell death. This evidence concerns the gene BCL2 and neoplasm.