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Dual inhibition of the MEK-ERK pathway (classical tumor signaling pathway) and Gln metabolism can induce redox stress, as evidenced by reduced mitochondrial membrane potential, elevated ROS levels, and inhibition of Gln degradation, and may be an effective therapeutic strategy for KRAS -driven NSCLC ( KRAS -driven cancer cells bypass the Gln-dependent G1 cell cycle checkpoint and are arrested in s-phase when Gln utilization is inhibited

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Weller M, Le Rhun E

However, in the cancer cells, the heightened level of ROS is countered by upregulated anti-oxidative defense mechanisms [4, 5]