In addition, the potential applicability of CRABP2 to potentiate RA FLS apoptosis is reinforced by the expression of Fas in the synovial lining5,6 and the finding that hydroxychloroquine, which is a weak disease-modifying anti-rheumatic drug (DMARD), potentiates Fas induced apoptosis of RA FLS54, and because therapeutic potentiation of the Fas pathway has consistently been found beneficial in both animal arthritis models and in human RA FLS55. The gene discussed is FAS; the disease is rheumatoid arthritis.