For example, the methylation status of the HOTAIR downstream intergenic CpG island is positively correlated with HOTAIR expression in breast cancer.[77] Moreover, type I collagen, which is enriched in the tumor microenvironment, is reported to promote HOTAIR expression via Myc in lung cancer cells.[78] The expression of HOTAIR can also be induced by estrogen through estrogen response elements of the HOTAIR promoter.[79] These factors might contribute to the aberrant abundance of HOTAIR in tumor tissues. This evidence concerns the gene HOTAIR and lung carcinoma.