In senescent human fibroblasts, HOTAIR is upregulated and prevents premature senescence by causing rapid decay of targets Ataxin-1 and Snurportin-1 [44]. In cancer cell lines, HOTAIR depletion may be correlated with cell cycle arrest by decreasing S phase cells, inhibiting cell proliferation rate, and promoting apoptotic levels [45, 46]. The gene discussed is HOTAIR; the disease is cancer.