Tumor cells often develop acquired resistance to ALK inhibitors, resulting from secondary mutations in the patient’s kinase domain, gene amplification, and activation of alternative signaling pathways (e.g., EGFR, kit, IGF1R, etc.)and epithelial mesenchymal transformation (Spaans and Goss, 2014; Kong et al., 2019). Here, EGFR is linked to neoplasm.