Such a compensatory mechanism has been described in non-small cell lung cancer (NSCLC) cells: Treatment with the EGFR erlotinib inhibitor induced heterodimerization of insulin-like growth factor receptor/epidermal growth factor receptor, activated IGF-1R and downstream signaling mediators, which ultimately counteracted the antitumor action of erlotinib in NSCLC cells [63]. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.