Hypothetical model in which DGKζ could negatively regulate 7TMR signaling. Upon activation of the 7TMR, β-arrestin is recruited to the receptor along with its bound DGKζ. The DGK terminates DAG signaling by converting this lipid to PA. The PA, in turn, might serve to activate a PtdIns4P 5-kinase (PI5K), which generates PtdIns(4,5)P2. This lipid promotes internalization of the 7TMR to limit access to its ligand.