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Mitochondrial GSH sequesters copper, preventing its binding to lipoylated proteins, such as DLAT, thereby blocking the aberrant protein oligomerization that drives this cell death pathway [109]

VEGF-neutralizing mAbs are designed to bind circulating VEGF and prevent its interaction with its receptors, thereby inhibiting the development and growth of new blood vessels [153]

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and (ii) off-target resistance caused by the activation of bypass signal transduction resulting from the amplification of the ERBB family of receptor tyrosine kinase genes, BRAF amplification, KRAS amplification, and KRAS mutations [148]