Moreover, the therapeutic efficacy of ACT appears to be limited by immune-evasion mechanisms within the tumor-bearing host, such as secretion of transforming growth factor beta (TGFβ) by the tumor microenvironment and/or accumulation of regulatory T cells (Treg), both of which severely dampen in vivo activation, expansion, and tumor homing of transferred tumor-reactive CD8+ T cells. Here, TGFB1 is linked to neoplasm.