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Among tyrosine kinase inhibitors, imatinib (a PDGFR inhibitor) and erlotinib (an EGFR inhibitor) induce ROS-dependent apoptosis in melanoma and non-small-cell lung cancer cells, respectively, through disruption of mitochondrial membrane potential upon the stimulation of JNK and p38 phosphorylation 88,89 , while vemurafenib (a BRAF inhibitor) increases the production of superoxide anions with the commensurate depolarization of the mitochondrial membranes in melanoma cells 90