In breast cancer, it has been shown that blocking TGF-β signaling in CD4+ T cells via a bispecific receptor that attaches the TGF-β-neutralizing TβRII extracellular domain to ibalizumab (a non-immunosuppressive CD4 antibody) causes a remodulation of the tumor microenvironment, and suppresses tumor growth [140]. This evidence concerns the gene TGFBR2 and neoplasm.