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doi: 10.1016/j.mrrev.2014.04.003 115 LashL

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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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Hence, these interconnected processes such as bacterial infections, mucus obstruction, inflammation, and structural airway damage highlight the multifactorial nature of CF pathogenesis, resulting in the progressive decline in pulmonary function [25]