HOTAIR could shift polycomb-group protein 2-mediated gene repression from tumorigenic genes to tumor-suppressive genes [17], it could interact with E3 ubiquitin ligases and their corresponding substrates through specific RNA binding domains to proteolyse oncogenes Ataxin-1 and Snurportin-1 [18], and it also could interact with several miRNAs that played positive or negative roles in tumor development [19,20]. The gene discussed is HOTAIR; the disease is neoplasm.