Concerning targeted therapies, several promising molecular targets have been suggested which, however, still await clinical transfer in the future: For example, in non-human primates, blockade of the central complement component C3 after trauma/hemorrhagic shock improved signs of TRAKI [104] and reduced the damage-driving TNK-1 [105], and similarly improved AKI in a septic shock model where C3-blockade reduced microthrombi within the glomeruli [106]. This evidence concerns the gene C3 and septic shock.