In this study, we aim to explore the EGFR-mutation induced drug resistance mechanism through the perspective of EGFR-RTK crosstalk (heterodimerization), and we considered ErbB2 (amplification frequently occurs in NSCLC), c-Met and IGF1-R as partners for mutated EGFRs. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.