Additionally, inflammation promotes TP53-associated clonal dominance, and TP53 heterozygous hematopoietic stem cell/progenitor cells from pre-TP53-secondary AML showed the increased expression of oxidative phosphorylation, DNA repair and interferon response genes without further modifications in levels of IFN receptor expression or concurrent IFN treatment [103]. Here, TP53 is linked to acute myeloid leukemia.