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Mutations in KEAP1 or the augmentation of SQSTM1 (sequestosome 1)-mediated KEAP1 protein degradation can enhance the stability of NFE2L2 protein, enabling cancer cells to evade ferroptosis and acquire drug resistance [34]

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Specifically, linking ONs - such as antisense oligonucleotides (ASOs) or short-interfering RNAs (siRNAs)to proteins or peptides can enhance properties like cell-specificity and cellular uptake 6 , which remain significant hurdles for many ON therapeutics

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