This mechanism might be particularly important when tumor cells escape CD8 T cell attack by alteration of MHC class I expression; these “immune escape variants”, are seen commonly in tumor cells [39], Although some tumor cells do not express MHC class II molecules, IFN-γ secretion by T cells and NK cells in an inflammatory environment in tumor sites could up-regulate MHC class II expression and render tumor cells susceptible to CD4 T cell killing. The gene discussed is CD4; the disease is neoplasm.