A second rebiopsy from the left adrenal gland displayed the original founder EGFR ex19del and the TP53 mutation (p.K320*) as well as three acquired potential mechanisms of TKI-resistance mechanisms: mutation of the NF2 tumor-suppressor gene (p.S87*) and high-level amplification of EGFR and MET genes (both >10 copies by NGS and 100% of tumor cells with MET gene “clusters” of >15 copies as assessed by FISH and resulting in MET-IHC 3+ in 100% of tumor cells). This evidence concerns the gene MET and neoplasm.