“…( 5 , 10 , 12 ) Resistance to imatinib can be multifactorial, presenting problems in the drug pharmacokinetics, mediators of cellular drug uptake, like the human organic cation transporter 1 (hOCT1) protein and mutations. Mutations are more frequent in secondary rather than primary resistance, ( 9 ) with the most common being deletion of BCR-ABL by amplification of this oncogene, mutation of the binding site of BCR-ABL by altered metabolism of imatinib, and by a transport mechanism. ( 5 , 10 , 12 ) Since 2001 with the first report of a mutation in resistant patients, more than 70 others have been reported.…”