EGFR非相关耐药机制中,研究指出:间质表皮转化(mesenchymal-epithelial transition, MET)和人表皮生长因子受体2(human epidermal growth factor receptor 2, HER2)的扩增[8]、RAS突变[21]、BRAF突变、1-磷酸酰肌醇-3-激酶(phosphatidylinositol 3-kinase, PIK3CA)突变、磷酸酶和张力蛋白类似物(phosphatase and tensin homolog, PTEN)缺失[9]、胰岛素样生长因子受体1(insulin-like growth factor 1 receptor, IGF1R)上调[22]、成纤维细胞生长因子受体(fibroblast growth factor receptor, FGFR)信号通路异常[8]、小细胞肺癌(small cell lung cancer, SCLC)转化[23]、上皮间质细胞转化[24](epithelial mesenchymal transition, EMT)、细胞周期基因改变[8, 9]、致癌基因融合[8, 9]、Bcl-2样蛋白11缺失、极光激酶A的激活、Src通路激活、整合素-kras复合物的形成、AXL的激活、EPHA2过表达[25-31]等均导致耐药。. This evidence concerns the gene PTEN and small cell lung carcinoma.