It was reported by Yano, S et al. that unlike the MET amplification, HGF-induced MET activation, acting as a specific mechanism of gefitinib resistance in lung adenocarcinoma harboring EGFR-activating mutations, motivated the PI3K/Akt signaling in an ErbB3-independent manner [34]. The gene discussed is HGF; the disease is lung adenocarcinoma.