Abstract

The arguments presented by Zong et al.1, 2 on the controversial role of P-glycoprotein (P-gp) are relevant. We agree that there is no evidence at present that this transporter represents per se a major resistance factor in vivo. In fact, in our recent clinical study we have shown that the MDR1 (ABCB1) 3435C>T polymorphism, associated with altered P-gp expression, tends to influence imatinib systemic pharmacokinetics, albeit not significantly.3 P-gp probably contributes to resistance but is not solely responsible for that.

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