This relative failure to upregulate IL-10 in response to IL-6 is in line with our earlier suggestion of a failure of RA macrophages to switch to the anti-inflammatory M2c phenotype, which is responsible for IL-10 release [3] as well as our recent study in CIA rats, which demonstrated decreased IL-10 concentration in muscle to be a robust marker for rheumatoid cachexia in this model [24]. The gene discussed is IL6; the disease is rheumatoid arthritis.