In a variety of tumor cells, stimulation with IFN-γ increases the expression of MHC II through the activation of CIITApIV (12), while hypermethylation and deacetylation were shown to block the inductive effects of IFN-γ on CIITA in promyelocytic cells and breast cancer cells (38,39), which thereby enabled tumor cells to evade immune surveillance. Here, IFNG is linked to neoplasm.