The cell line studies corroborated the clinicopathologic findings well and suggested that JARID1B may facilitate the oncogenic network of events through the epigenetic modulation of epithelial-mesenchymal transition (EMT) regulators including vimentin, snail, and E-cadherin, plus upregulation of a subset of pluripotent transcription factors such as OCT4, SOX2, KLF4, and c-Myc, and finally contribute to aggressiveness and stemness of NSCLC cells. The gene discussed is MYC; the disease is non-small cell lung carcinoma.