As such, future endeavors to not only target Rep2‐dependent activation of mTOR in NSCLC but also determine the relevance of this mechanism in other cancer types, including cross‐talk of the NRF2‐Rep2 axis with other key survival pathways, could provide a novel therapeutic approach to treat cancers that rely on increased NRF2 and mTOR function for survival. Here, CHML is linked to cancer.