Future studies, therefore, have to address the limitations of our present study and (i) investigate the complexity of AML also in the uncommon erythroid, megakaryocytic, and myelofibrotic AML variants that were not present among our patients (see Table 1), as well as (ii) additional post-translational modulations and/or the presence of various proteoforms that may differ between leukemic and normal CD34+ cell and/or between AML patient subsets. This evidence concerns the gene CD34 and acute myeloid leukemia.