Furthermore, treatment with the EGFR-TKI (AG1478) inhibited miR-21 expression in two NSCLC cell lines with elevated p-EGFR, EGFR-mutant H3255, and EGFR wild-type H441, providing a mechanistic link between an activated EGFR signaling pathway and the aberrant up-regulation of miR-21, and a therapeutic basis for the inhibition of miR-21 in lung cancers with EGFR activation. The gene discussed is EGFR; the disease is non-small cell lung carcinoma.