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Mutations resulting in the suppression of complex II in hereditary pheochromocytoma/paraganglioma and renal cell carcinoma elicit elevated ROS generation and reduce ATP synthesis by oxidative phosphorylation [17, 18]

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However, mutant EGFRs differ from their wild-type counterparts in their subcellular localisation [38], which probably results in the EGFRm/T790M having different signalling partners as EGFRm or wild-type EGFR