Resistance to chemotherapy is a serious problem in successful treatment of malignancies, including MDS and AML. The failure of treatment may be due to the development of multidrug resistance (MDR) phenotype. Multidrug resistant neoplastic cells exert reduced sensitivity to more than one drug that differs in structure and pharmacological efficiency. MDR represents the induction of large-scale defensive mechanisms including up-regulation of membrane transporters (like P-glycoprotein – P-gp), drug metabolism, alterations in drug-induced apoptosis, epigenetic changes, epithelial-mesenchymal transition, alteration in drug targets structures, and acceleration of DNA1 repair [ 4 , 3 ]. Mechanisms involved in the development of multidrug resistance could act independently or could cooperate. One of the most observed molecular causality of MDR is up-regulation of membrane transporters (like P-glycoprotein – P-gp) effluxing chemotherapeutic drugs from tumor cells. P-gp belongs to ABC transporters (ATP -binding cassette Transporters) that utilize the energy of ATP binding and hydrolysis to transport various substrates across cellular membranes. P-gp could efflux a large scale of different uncharged substances from cells. Different drugs like colchicine, tacrolimus, and quinidine; chemotherapeutic agents such as etoposide, doxorubicin, and vinblastine; different lipids and steroids; xenobiotics; DNA-intercalators such as ethidium bromide; linear or circular peptides like valinomycin and gramicidin; bilirubin; cardiac glycosides like digoxin; different immu‐nosuppressive agents; glucocorticoids like dexamethasone; HIV-type 1 antiretroviral therapy agents like protease inhibitors and nonnucleoside reverse transcriptase inhibitors; and many others are known to be P-gp substrates [ 4 ]. Therefore, research of multidrug resistance phenomenon is really necessary for improvement of cancer treatment.