Indeed, the overexpression of miR-21 led to a significant decrease of gefitinib sensitivity in PC9 lung cancer cells through a mechanism by inhibiting PTEN expression and activating the Akt/Erk signaling pathway, while knockdown of miR-21 dramatically reversed gefitinib sensitivity in PC9GR cells by upregulating PTEN and inactivating the Akt/Erk pathway, suggesting modulation of miR-21/PTEN expression may be a promising strategy for resensitizing EGFR-TKI resistance in NSCLC [33]. This evidence concerns the gene AKT1 and lung cancer.