This conclusion is further supported by our previous observations of a decreased level of GARP on Tregs from patients with rheumatoid arthritis.26 Moreover, for atopic dermatitis, a significant excess of low-frequency missense mutations in LRRC32 leading to low GARP expression has been reported.27 Finally, it has been shown that Garp-deficient Tregs facilitate antitumor immunity but are unable to suppress pathogenic T cell responses in a T cell transfer model of colitis, pointing once again to impaired suppressive Treg function in the absence of GARP.28 Here, LRRC32 is linked to atopic eczema.