The importance of CD16 receptor function in the development of sarcoidosis may be highlighted by the fact that the anti-sarcoidosis treatment with prednisone (an immune-suppressive glucocorticoid medication) and infliximab (IgG1 monoclonal antibody against tumor necrosis factor alpha) have been shown to downregulate pro-inflammatory intermediate (CD14+CD16+) and non-classical (CD14−CD16++) monocytes, and not the classical CD14+CD16− monocytes. This evidence concerns the gene FCGR3A and sarcoidosis.