Immune escape is usually associated with loss of stimulating molecules that includes the downregulation of classical HLA molecules (missing self-hypothesis), loss of stimulatory cytokines, and/or gain of suppressing molecules such as expression of nonclassical HLA-G, functional Th2-type activity shift (e.g., decrease in IFNγ and/or increase in TGFb, IL6, and IL10) and elevation of the Fas ligand on cancer cells [14,15,16]. The gene discussed is FASLG; the disease is cancer.