PGP and neoplasm: The precise mechanisms by which these components interact with irinotecan are not fully understood, but several hypotheses have been proposed [32]: (i) maintaining high circulating levels of irinotecan by inhibiting P-gp efflux, (ii) enhancing selective delivery of irinotecan to tumor cells, (iii) boosting immune response and inducing direct DNA damage through apoptosis, (iv) altering the metabolic activation of irinotecan, and (v) the synergistic action of flavonoids and chemotherapeutic agents on topoisomerase I and II.