The bulk of this work is the description of myelopoiesis, differentiation pathway from the myeloid precursor to the final lineage of granulocytes (neutrophils, eosinophils, basophils) and agranulocytes (monocytes/macrophages). Disruption of differentiation mechanisms, as inhibition of lineage-specific differentiation factors and biosignalisation pathways Ras/Raf/MEK/ERK and PI3K/Akt/mTOR/S6K leads to excessive formation of immature cells, where they accumulate in the bone marrow and the bloodstream, so it all results with leukemia. Otherwise, APL is described as a disease with a fatal outcome within only a few weeks after diagnosis and is characterized by a balanced reciprocal translocation between chromosomes 15 and 17. The result is a fusion between PML gene and retinoic acid receptor α (RARα) which causes a conformational change whereby co-repressor HDAC remains bound to this newly synthesized hybrid protein PML/RARα at physiological concentrations of RA. The final consequence is an increased proliferation of abnormal promyelocytes. All that leads to disruption of normal differentiation toward granulocytes. However, a clinical application of ATRA and ATO in APL treatment achieved a considerable success. Importanly, ATRA and ATO properties such as enhanced modification or degradation of PML/RARα oncoprotein, mediated by intracellular caspases and a cytoplasmic complex proteasome, might provide a plausible explanation for the appreciable efficacy of this combination therapy in APL patients.