Similarly, we confirmed that miR-200c, which is highly expressed and associated with epithelial–mesenchymal transition, invasion, and migration in NSCLC patients [44], was inhibited by G9a in A459 cells measured based on small RNAseq analyses, indicating that G9a not only regulated HER3 through the repression of miR-145-5p expression but also increased other oncogenes, such as the astrocyte leptin receptor, through the repression of miR-200c expression, which enhanced tumorigenesis in lung cancers. The gene discussed is LEPR; the disease is lung carcinoma.