Strategies targeting MCL‐1 and BCL‐XL, including use of inhibitor R‐roscovitine, a cyclin‐dependent kinase (CDK) inhibitor that reduces MCL‐1 protein levels and triggers neutrophil apoptosis, have successfully ameliorated arthritis in mouse models.[41, 42] Neutrophils exhibit high sensitivity to FAS ligand (FASL)‐induced apoptosis and elevated levels of TNF‐α. The gene discussed is FASLG; the disease is arthritic joint disease.