It has been shown that GARP binds latent TGF-β and the function of sGARP is TGF-β receptor dependent and leads to Smad2/3-phosporylation.[9] TGF-β1 influences a variety of immune cells and consequently these cells express TGF-β receptors, with the TGF-βRII playing a central role in signaling.[35] Apart from having identified sGARP as important promoter of Treg function and regulator of peripheral T helper cell activity, [9] sGARP is a product of Treg and melanoma cells themselves (the present study). Here, SMAD2 is linked to melanoma.