Several studies have demonstrated abnormalities in BM-derived MSCs isolated from people with systemic lupus erythematosus (SLE-MSCs), including differential expression of a total of 1905 genes.25 Gu et al reported that SLE-MSCs had slower rates of proliferation and increased β-galactosidase (β-GAL) expression consistent with premature senescence.28 They also showed that p16INK4A, a tumor suppressor that inhibits the cyclin-dependent kinases CDK4 and CDK6, was significantly upregulated in SLE-MSCs. Here, CDKN2A is linked to systemic lupus erythematosus.