Previous studies showed that Mer was required for surface accumulation of EGFR and subsequent pathway activation in lung cancer cells [39]; thus, it is tempting to speculate that Mer might maintain the persistent activation of the key prosurvival PI3K/AKT signaling pathway in NSCLC cells with EGFR mutation exposed to erlotinib by the direct (activating AKT signal) and/or indirect (sustaining EGFR signal) mechanisms, convergently leading to the resistance of NSCLC cells to erlotinib. This evidence concerns the gene AKT1 and lung cancer.