For instance, HOTAIR was upregulated in small cell lung cancer multidrug-resistant cell lines (H69AR and H446AR), and depletion of HOTAIR enhanced H69AR and H446AR cell sensitivity to anticancer drugs through increasing cell apoptosis and cell cycle arrest by inhibiting DNMT1 and DNMT3b expression and reducing HOXA1 methylation [20]. This evidence concerns the gene HOXA1 and small cell lung carcinoma.