These divergent effects may explain the inconsistency in the clinical efficacy of different anti-CD4 mAbs particularly in the treatment of rheumatoid arthritis, namely a promising initial efficacy in open anti-CD4 trials [30,31], subsequent discouraging double-blind clinical trials (reviewed in [32]), and, finally, a revitalization of the anti-CD4 treatment notion with new, humanized anti-CD4 mAbs [33]. The gene discussed is CD4; the disease is rheumatoid arthritis.