On one side, EGFR targeting can be considered to be the highest example of oncogene addiction in NSCLC; currently, it is clear that the majority of EGFR activating mutations can be efficiently treated with the third-generation EGFR-TKI osimertinib [20], which, however, develops resistance mechanisms through MET activation, EMT features and alterations in cell-cycle and DDR-related proteins [21]. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.