Prominent mechanisms of drug resistance in AML are supported by diminished intracellular daunorubicin retention directed by P-gp, reduced capacity of the activating enzyme deoxycytidine kinase, and overexpression of the inactivating cytoplasmic 5′-nucleotidase II [108], the entry of sphingolipid metabolism into the blend adds a new dimension with possible therapeutic implications. The gene discussed is PGP; the disease is acute myeloid leukemia.