To translate the relevance of these observations to human disease, we first examined the expression of hMICL in the synovium of patients with RA and controls, using monoclonal antibodies which are specific for human MICL.6 Immunohistochemical analysis disclosed the presence of hMICL in the synovial lining layer and in scattered subsynovial cells of patients with RA, but that there was little or no expression in non-inflamed synovium (figure 4A). This evidence concerns the gene CLEC12A and rheumatoid arthritis.