For example, in non-small-cell lung cancer (NSCLC) and ovarian cancer, the E-to-M transition switches the dependence of carcinoma cells from the EGFR to the AXL receptor tyrosine kinase, thereby yielding resistance to EGFR-targeted therapy (Fig. 3B) [69,70]. This evidence concerns the gene EGFR and non-small cell lung carcinoma.