In a follow-up paper, Liu et al., using the MNP model on HSCs harboring the 11B3 chromosomal deletion–a 4 Mb region on mouse chromosome 11 that is syntenic to human 17p13.1 [97], showed that 11B3 deletion promoted the development of more aggressive AML compared to the p53-null background, suggesting that other genes than TP53 drive the selection for 17p loss during leukemogenesis [97]. The gene discussed is TP53; the disease is acute myeloid leukemia.