Notably, distinct from heterogenous p53EE stabilization in spontaneous tumors (Figs 6C and EV5), p53EE was highly accumulated in all lymphomas from Eμ‐Myc;p53EE/+ mice and in all AE9+Nras;p53EE/EE AML samples (Fig 6F and G). This evidence concerns the gene MYC and acute myeloid leukemia.