An example to support this assumption is the study by Visser and co-authors who employed ex vivo system to demonstrate that CD4+CD25high Tregs can inhibit IFNγ production by stimulated HPV16 E6/E7-specific Т cells isolated from peripheral blood of CIN and cervical cancer patients [15]; nonetheless the spectrum of relationships between CD4+Tregs and their potential target cell populations formed upon CIN/CC development remains largely uncharacterized. The gene discussed is IFNG; the disease is cervical cancer.