Soluble Fas (sFas) levels in RA joints have been reported to be elevated and inhibit membrane-bound Fas (mFas) by activating the extracellular signal-regulated kinase (ERK) 1/2, phosphatidylinositol 3-kinase (PI3K), caspase-8, and c-Jun N-terminal kinase (JNK) signaling pathways to enhance the anti-apoptotic effect of FLS. The gene discussed is FAS; the disease is rheumatoid arthritis.