SH2D2A and systemic lupus erythematosus: These cells also show decreased phosphorylation of signaling molecules (i.e. Zap-70, LAT and PLCγ1) [7], which could be due to poor activation of Lck in the absence of SH2D2A. With age, SH2D2A-deficient mice develop a lupus-like autoimmune disease, which has been suggested to be associated with defective T cell death in vivo[13].