Conversely, the under-expression of lncRNA DILC in RA, and the subsequent overexpression of DILC, has been suggested as a strategy to ameliorate RA by downregulating interleukin-6 (IL-6) and inhibiting fibroblast-like synoviocytes (FLSs) apoptosis [14]. The gene discussed is IL6; the disease is rheumatoid arthritis.