AML cells operate under chronic replication stress driven by oncogenic signaling (e.g., FLT3, RAS), rapid cycling, and dysregulated nucleotide metabolism, rendering adverse-risk clones—such as those with complex karyotypes or TP53 aberrations—checkpoint-addicted (Quintás-Cardama et al., 2017). This evidence concerns the gene TP53 and acute myeloid leukemia.