These experimental results indicate that, in effector cells from different autoimmune disorders with specific target organs, distinctive expression of p53-dependent lncRNA such as lincRNA-p21 in SLE pulmonary cells and H19 in RA synoviocytes can modulate the apoptotic process, resulting in accelerated and receded cell apoptosis, respectively, to perpetuate the disease activity. This evidence concerns the gene H19 and rheumatoid arthritis.