These include increased DNA repair, formation of trapping agents (e.g., some tumor cells produce glutathione which can trap and thereby inhibit activity of certain anti-cancer drugs), alterations in target molecules, decreased activation of prodrugs, inactivation of anticancer drugs, decreased drug accumulation (e.g., due to increased expression of P-glycoprotein (MDR1)), and increased expression of pro-survival molecules. The gene discussed is ABCB1; the disease is cancer.