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Several studies have identified various sources of ROS and RNS in IBD, including neutrophils, macrophages, and inflamed intestinal tissue ( 2 Mechanism of oxidative stress in IBD While the precise mechanisms responsible for the development of IBD remain unclear, it is widely accepted that multiple factors contribute to its etiology, including overproduction of ROS, damage to biomolecules, mitochondrial dysfunction, recruitment of immune cells, impaired antioxidant defense system, and the activation of inflammatory pathways ( Figure 1 )

Separately, the copper-exporting ATPase ATP7B has been implicated in cisplatin resistance via small extracellular vesicles (sEVs)

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It has been reported that tumour-derived exosomes polarise M towards an immunosuppressive phenotype through NF-B-dependent metabolic reprogramming, which further increases PD-L1 expression [95, 215]