Our findings support a model, in which the intrinsic apoptotic defect in TP53-deficient AML/MDS cells results in a longer duration of the cellular interaction between CAR T-cells and TP53-deficient AML/MDS cells as shown by indirect as well as direct evidence of enhanced trogocytosis and live-cell imaging, respectively. Here, TP53 is linked to myelodysplastic syndrome.