It has been suggested that Tregs defect in DOCK8 deficiency occurs through the breakdown of their interaction between the Wiskott–Aldrich protein (WASP) and WASP-interactin protein (WIP), or the activation of STAT3.[13,14] Recently, it has been shown that DOCK8 regulates the suppressive activity of Treg cells through interleukin (IL)-2 in STAT5 signaling.[15] As observed in DOCK8 deficiency, defective Treg cells play a role in the pathogenesis of SLE. This evidence concerns the gene WAS and systemic lupus erythematosus.