Another recent study reported that a mouse model deficient in RORγt (a transcription factor required for Th17 differentiation) exhibited accelerated growth of transplanted melanoma tumors, along with a diminished percentage of Th1 CD4+ cells at the tumor site; this phenotype was rescued by adoptive transfer of Th17 cells, a portion of which began to produce measurable quantities of IFN-γ (41). Here, IFNG is linked to neoplasm.