Recently, it was demonstrated that EGFR signalling pathways were activated by autocrine EGF and TGF-α and withstood c-Met and anaplastic lymphoma kinase (ALK) inhibition leading to primary and acquired resistance to TAE684/SGX-523 (ALK/c-Met inhibitors) in NSCLC [40]. This evidence concerns the gene ALK and non-small cell lung carcinoma.