Further validation in larger, randomized trials will be needed to confirm and better define the mechanisms of AML-induced T-cell dysfunction and to clarify whether the limited efficacy of TTCR-C4 in this study reflects an insufficient therapeutic effect of WT1 targeting in active disease or whether cellular therapies are generally less effective in this setting compared to the prophylactic context13. The gene discussed is WT1; the disease is acute myeloid leukemia.