AML is characterized by a diverse array of genetic mutations that affect key pathways, including signal transduction (FLT3), epigenetic regulation (DNMT3A, IDH1/2, EZH2), and apoptosis (TP53).4 These mutations drive distinct transcriptional programs, contributing to variability in disease behavior and drug sensitivity.142 Additionally, chromosomal translocations (e.g., t(8;21), inv(16), t(15;17)) further influence AML prognosis and treatment strategies. Here, TP53 is linked to acute myeloid leukemia.