The latter capacity may be imparted via diverse mechanisms [17], [18]: (i) tumor cells can lose their MHC class I molecules, enabling them to evade CTL attacks [19]; (ii) while the immunodominant epitope becomes the main target of immune responses, cells with other phenotypes may continue proliferating in the “shadow” of the dominant clone [20]; (iii) furthermore, tumor cell secretion of immunosuppressive cytokines such as TGF- and IL-10 can reduce the efficiency of the immune response [21], and (iv) a modification of death signaling may prevent cells from undergoing apoptosis [22]. Here, IL10 is linked to neoplasm.