We previously observed that BM-MSCs from SLE patients showed increased expression of p16INK4A, knockdown of p16INK4A expression increased proliferation capacities, and decreased SA-β-gal activity; it suggested that cell cycle relation protein p16INK4A was involved in the cellular senescence process of BM-MSCs from SLE patients. The gene discussed is CDKN2A; the disease is systemic lupus erythematosus.