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In heterogeneous tumor environments, achieving selective targeting of mutant p53 cells without damaging wild-type p53-dependent normal cells is a major challenge, mainly for the following reasons: some drugs targeting mutant p53 may also be toxic to wild-type p53 cells, and the complex tumor microenvironment may affect the efficacy of drugs

Terpstra, A

The observed failure of drugs targeting S-glutathionylation in clinical trials regarding ovarian cancer might be explained by resistance mechanisms such as increased/decreased rates of drug efflux/influx as cellular redox status affects transporters function or resistance to apoptosis through caspase-3 S-glutathionylation [73]

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