Tumor cell death inducing therapies promote inflammation, hypoxia, ROS production and may additionally activate the Phoenix rising - caspase-3- cytosolic phospholipase A (2) alpha (cPLA-2)-COX-2-PGE-2-STAT3 pathway to reestablish compensatory tumor regrowth by establishing all disease traits described with M-CRAC (12, 71–73). The gene discussed is STAT3; the disease is neoplasm.