It has been shown that mice prone to lupus nephritis exhibit Treg instability due to diminished Foxp3 expression.41 Moreover, associations between diminished Foxp3 expression and human immune disorders have been shown.42,43 Thus, taken together, our data demonstrate that in the absence of GARP, Tregs develop signs of TGFβ1 deprivation characterized by increased expression of Hdac9 and subsequent destabilization of Foxp3, resulting from reduced acetylation. The gene discussed is LRRC32; the disease is lupus nephritis.