For example, mAbs targeting CCR4, a chemokine receptor heavily involved in Treg recruitment to the TME, have shown promising results in clinical and laboratory studies, effectively depleting activated FoxP3+CCR4+ Tregs with only a limited impact on tumor-infiltrating Teff and CTL subsets [41,45,67,68,69,70]. The gene discussed is CCR4; the disease is neoplasm.