“…These authors also show that the aggressive tumours developed in NKG2D-deficient mice express higher levels of NKG2D ligands (which mediate NK-mediated destruction of some tumour cells) than the tumour cells from wildtype mice, suggesting that in immunocompetent mice one of the early events in the immunoediting of spontaneous tumours may be the selection of tumour-cell variants that express low levels of NKG2D ligands. The hypothesis that both spontaneous and virally induced tumours can be recognised and controlled by the immune system is now clearly supported both by clinical and laboratory data (Farge, 1993;Curtis et al, 1997;Luppi et al, 2000;Scadden, 2003;Kasiske et al, 2004;Kannagi, 2007;Lagos et al, 2007). Furthermore, the idea that tumour development in an immunocompetent animal proceeds through a variable sequence of immunologic checkpoints involving tolerance induction, immunoselection, immune evasion and/or immune elimination has been well supported by experimentation with 3-MCA-induced sarcomas (van den Broek et al, 1996;Kaplan et al, 1998;Smyth et al, 1999;Shankaran et al, 2001;Dunn et al, 2002;Koebel et al, 2007).…”