Of note, pDC differentiation was identified solely in cases of AML-MR and was conspicuously absent among cases of AML-MR with TP53 mutations (all of which were associated with RUNX1 copy number gain) and AML post-cytotoxic therapy (all of which harbored TP53 mutations and RUNX1 copy number gain, with one case demonstrating an additional RUNX1::CBFA2T3 rearrangement), likely reflecting a different pathobiology driven by TP53 aberrations and impacting the clonal architecture in these cases. The gene discussed is RUNX1; the disease is acute myeloid leukemia.