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Collectively, targeted inhibition of SUV39H1 demonstrates efficacy in attenuating post-injury neointima formation, positioning it as a novel therapeutic candidate for proliferative vasculopathy including in-stent restenosis (31)

As our work does not conclusively indicate the cause-effect of increased GSH levels towards ethanol titres, we cautiously conclude that there is a limit to cellular fitness that could be accomplished via increased levels of glutathione

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This intrinsic plasticity underlies not only the rapid emergence of resistance, the persistence of tumor heterogeneity, and the adaptive evolution of cancer