In vitro studies analysing potential combination therapies on both head and neck SCC and NSCLC cell lines suggest that there is also antagonism between gefitinib and cisplatin in other tumour types [25–27]; the effects have been variously attributed to cisplatin cytotoxicity being dependent on EGFR phosphorylation and degradation [28], induction of epithelial to mesenchymal transition (EMT) which is associated with increased resistance to gefitinib [26], reduced cisplatin entry into the cell and increased DNA repair or cell cycle arrest in G1. The gene discussed is EGFR; the disease is neoplasm.