Synovial hyperplasia is the primary pathological changes of RA and FLS is the principal etiological cellular component that drives and constitutes the pathological lesions. To elucidate the molecular mechanism of how FLS may contribute to RA, we performed transcriptome profiling to determine the DEGs between normal and RA FLS. We compared the primary FLS isolated from healthy control (HFLS) to that isolated from RA patients (RA FLS), and also to an immortalized RA FLS cell line MH7A immortalized by stably transfecting primary RA FLS cells with SV40 T antigen gene.