Although a number of studies revealed that a variety of mechanisms can stimulate acquired resistance to EGFR-TKI including secondary mutations within EGFR at position T790, mutation in EGFR effector proteins, small-cell lung cancer histologic transformation and upregulation of parallel receptor tyrosine kinases (e.g., MET, HER2 and AXL) [4], the mechanisms responsible for about 20–30% of cases of acquired resistance to EGFR-TKIs are still unknown. This evidence concerns the gene AXL and small cell lung carcinoma.