In line with this evidence, Fu et al. have shown that mice with a T cell–specific deletion of PLC-γ1 were characterized by impaired generation and function of Treg cells and developed autoimmune disease; on the contrary, enhancement of diacylglycerol-mediated signaling, a second messenger produced by activated PLC-γ, has been shown to increase Treg cell suppressive activity (35, 36) (Fig. 1). Here, PLCG1 is linked to autoimmune disease.