Finally, increased miR-497 level was seen to have a significant impact in enhancing sensitivity to EGFR-TKI in NSCLC cells via IGF1R targeting and AKT activation (90), whereas in vitro experiments and in vivo models were useful to demonstrate that the combination of gefitinib plus a microRNA mimic, miR-30a-5p, could overcome acquired EGFR-TKI resistance in NSCLC via a direct regulation of IGF1R and HGFR (hepatocyte growth factor receptor) signaling (91). The gene discussed is AKT1; the disease is non-small cell lung carcinoma.