A similar mechanism of immune evasion involves AML cells that induce the accumulation of regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs) in the tumor microenvironment, which can inhibit CAR-T cell activity through direct cell-to-cell contact, metabolite secretion (including reactive oxygen species and nitric oxide), or cytokine-mediated suppression (including IL10 and TGF-β) [46]. The gene discussed is TGFB1; the disease is neoplasm.