Mechanisms employed by the tumor in this phase can be distilled into the following three categories:16 (1) reduced immune recognition and immune cell stimulation by downregulation of tumor antigens, antigen-expression machinery or co-stimulatory signals—all required for successful activation of APCs and thus T-cells, (2) upregulation of resistance against cytotoxic immunity or upregulation of pro-tumorigenic genes (e.g., STAT3 or Bcl2, respectively), and (3) creation of an immunosuppressive microenvironment. The gene discussed is BCL2; the disease is neoplasm.