Although genetic disruption of pro-apoptotic protein BID or BIM aggravates arthritis in K/BxN mouse model (Scatizzi et al., 2006; Scatizzi et al., 2007) and BH3 domain mimetic peptide treatment has also been reported to ameliorate arthritis development (Scatizzi et al., 2010), the underlying mechanism and targeting cell type are not known. This evidence concerns the gene BCL2L11 and arthritic joint disease.