During treatment with chemotherapy drugs, many cancers become resistant to the therapeutic effects of the drugs used. Various mechanisms have been proposed in relation to drug resistance. One of the most important reasons for drug resistance is the high expression of ATP-dependent membrane proteins from the large family of membrane transporters (ATP Binding Cassette ABC). From this family, the membrane transporter with a molecular weight of 170 KDa named glycoprotein P plays an important role in drug resistance. Other membrane proteins from the MRP (Multidrug Resistance Associated Protein) family are also involved in drug resistance. ABC proteins are also expressed in normal cells. The mentioned proteins are responsible for the transfer of endogenous substrates. The high expression of these proteins in cancer cells is the most important obstacle to cancer treatment. The range of clinical responses is caused by the medicinal qualities of the treatment as well as the internal and acquired molecular and physical characteristics of cancer cells and external environmental factors. The latter can be caused by several factors, such as increased DNA repair capacity, altered drug metabolism, mutated or altered drug targets, reduced drug accumulation, and inactivated cell death signals. Cancer stem cells (CSCs) show drug resistance. Because transporters overexpress adenosine triphosphate (ATP) binding cassette. Through specific regulatory genes, FOXM1, a transcription factor specific for cell proliferation, controls the transition between G1/S and G2/M cell cycle phases. In addition, it is an oncogene that causes the expansion and proliferation of cancer cells. Via ABCC5 (ATP binding cassette subfamily member 5) expression, FOXM1 overexpression causes paclitaxel resistance in nasopharyngeal carcinoma.