This is performed through the downregulation of growth hormone receptor (GH), the upregulation of the members of the SOCS family that negate the action of GH and an increased clearance of IGF-I through catabolism of IGF-I bindings proteins (IGFBPs).29 Our study contributes to this literature and assumes a possible role of IGF-I in the pathogenesis of RA sarcopenia. This evidence concerns the gene GHR and rheumatoid arthritis.