Altogether, these data clearly indicates that the malignant T cells become resistant to immunosuppressive factors (e.g., dysfunction of Fas-, IL-10-, and TGF-β-signaling and upregulation of SOCS3) while acquiring the capacity to inhibit anti-tumor immunity by means of cell contact-dependent (e.g., CD80, PD-L1, and FasL) and independent (e.g., Th2 cytokines, IL-10, TGF-β) mechanisms. This evidence concerns the gene IL10 and neoplasm.