Our proteomic analysis revealed that THZ-P1-2 resistant AML CD34+ (or CD117+ for NPM1-mut AMLs) cells displayed a molecular signature similar to L-HSC and TP53 mutant AML, with a more glycolytic-driven metabolism, whereas THZ-P1-2 sensitive AML samples displayed enrichment for cell maturation markers and mitochondrial metabolism, which corroborates the findings of our functional studies. This evidence concerns the gene CD34 and acute myeloid leukemia.