In the EGFR-mutated patient, activation of ERBB2, representing parallel or “bypass” signaling pathway that share downstream effectors with EGFR, has been demonstrated to make tumor cells less dependent on EGFR for activation of these downstream effectors, and thereby reduce the antitumor efficacy of EGFR-TKI.[4] There are target drugs available for Her2 positive patients resulting from ERBB2 amplification. Here, ERBB2 is linked to neoplasm.