FOXP3 and neoplasm: Most importantly, these results logically form a coherent mechanism chain: the combined treatment may directly or indirectly inhibit TGF-β1 in the tumor microenvironment, thereby weakening the expression of Foxp3, the “master switch” that drives the differentiation of naive T cells into Treg cells, ultimately leading to a reduction in Treg cells at both systemic (peripheral blood) and local (tumor tissue) levels and the alleviation of the overall immunosuppressive state.