to follicular lymphoma cells. This strategy triggered a potent NQO1-mediated redox cycle, resulting in severe NADH depletion and profound oxidative stress. These events activated the GADD45β-MAPK stress-signaling pathway, leading to mitochondrial dysfunction and apoptosis activation. In a murine FL xenograft model, this approach achieved 85% tumor growth inhibition, while maintaining a favorable safety profile. This work establishes a new therapeutic paradigm for FL, leveraging intrinsic enzyme deficiency to induce tumor-specific, self-amplifying cell death.
Zhang et al. (2026) studied this question.