Overexpressed NEAT1 in the G-MDSCs from the lupus murine model could lead to BAFF secretion and thus promote the activation of B cells so as to accelerate the progression of SLE, while the delivery of NEAT1 by PBMCs-derived exosomes could promote the development and progression of RA via the microRNA-23a/MDM2/SIRT6 axis (60, 128). This evidence concerns the gene NEAT1 and systemic lupus erythematosus.