Lastly, optimizing antigen selection (e.g., blasts- and LSC-restricted antigens) and improving bone marrow honing or stromal-penetration (e.g., via chemokine receptors, ECM-remodeling CARs) may increase CAR-T access to sanctuary sites where TP53 mutant AML clones survive. This evidence concerns the gene TP53 and acute myeloid leukemia.