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Indeed, NRF2 was found constitutively active in intestinal stem cell (ISC) in , and KEAP1-mediated NRF2 repression was required for ISC proliferation

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And it is worth noting that many KRas-dependent tumors develop resistance to mTORC1 inhibition by upregulating glutamine metabolism, but the combination of mTORC1 inhibition with CB-839 can overcome this resistance [110]

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