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 phosphorylation88,89, while vemurafenib (a BRAF inhibitor) increases the production of superoxide anions with the commensurate depolarization of the mitochondrial membranes in melanoma cells90. The gene discussed is EGFR; the disease is melanoma.