Several EGFR–independent mechanisms, including BRAF-V600E, KRAS mutations, oncogenic fusions (NTRK-, RET-, ALK-fusion), MET- and HER2-amplification/mutation, epithelial-to-mesenchymal transition (EMT), and cell type transformation (from NSCLC to SCLC) were reported to confer resistance to osimertinib [25,44,45]. The gene discussed is ALK; the disease is non-small cell lung carcinoma.