Interestingly, molecular analysis of serial patient samples has provided evidence that AML therapy induces evolutionary pressures for loss‐of‐heterozygosity and expansion of newly acquired double‐hit TP53 cell populations45, 46 Thus, AML patients initially presenting with mono‐allelic TP53 alteration may have similar clinical outcomes as patients with bi‐allelic TP53 alteration. The gene discussed is TP53; the disease is acute myeloid leukemia.