Considering the importance of GPCRs as drug targets [6] and the recent finding that the pharmacologic targeting of Adgrg3-mediated Sema3A signaling may provide an approach for AKI treatment [9], we will utilize inducible, conditional Gpr126 knockout mice in the future to determine whether the lack of Gpr126 improves or worsens the disease outcome in different kidney injury models and assess changes in the behavior of Gpr126-expressing cells and their neighboring cells. The gene discussed is SEMA3A; the disease is medical procedure.