For example, VanMeter et al. revealed an alternative mechanism of downstream protein activation, which is independent of EGFR in non-small cell lung cancer;154 Sergina et al. showed that overexpression of HER3 could lead to a compensatory shift in phosphorylation-dephosphorylation equilibrium, resulting in gefitinib resistance;155 Canfield et al. found that HER4 was upregulated in HER2+ breast cancer with lapatinib resistance, and knockdown of HER4 significantly decreased ATK phosphorylation levels, indicating the bypassing receptor function of HER4 in lapatinib-resistant cells.156. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.