Contrary to the role of chronic IFN-γ in MCA-induced carcinogenesis, the growth of the transplantable B16 tumor was significantly suppressed by IFN-γ in the same animal model, and these discrepancies could be attributed to the variations in duration of IFN-γ exposure (acute versus chronic), and quite possibly to the differences in tumor types [64]. Here, IFNG is linked to neoplasm.