MERTK and non-small cell lung carcinoma: Mechanistic investigation revealed that erlotinib treatment did not effectively inhibited AKT signaling in otherwise erlotinib-sensitive NSCLC cells upon Mer overexpression, suggesting that sustained AKT signal downstream of Mer activation mediated the erlotinib resistance as evidenced by recovered erlotinib sensitivity in Mer-overexpressed PC9 cells when concomitantly treated with an AKT inhibitor.