Previously, the expression of Bcl-2, a well-documented anti-apoptotic gene, was found to be inhibited while that of Bax, a well-documented pro-apoptotic gene and the apoptotic protease caspase-3 was increased when the signal transducer and activator of transcription 3 was suppressed, ultimately inducing RA-FLS apoptosis [28]. The gene discussed is BCL2; the disease is rheumatoid arthritis.