Lack of Tregs in Cd4-/- hosts also does not slow INHBA-driven growth of a papilloma virus-induced skin cancer model.18 At first glance, this is surprising since Activin-A can synergize with TGFβ to induce Tregs.39 40 However, Tregs only express Alk7, which preferably binds INHBB-derived Activins.24 The failure of melanoma cell-derived Activin-A to enrich Tregs or to increase CD4+ T cell-mediated immune evasion in any of our preclinical models points to its limited bioavailability in this cell type. This evidence concerns the gene CD4 and skin cancer.