Besides the expansion of naïve Treg cells through enhanced self-renewal and differentiation, other mechanisms have been proposed amongst them the interaction of CCR4 on Treg cells with CCL22 released in the tumor microenvironment [38] as well as the conversion of conventional CD4+CD25− T cells to Treg cells trough TGF-β [39] or prostaglandin E2 [40]. This evidence concerns the gene TGFB1 and neoplasm.