While in some cases dual targeting of PS receptors can compound phenotypic outcomes [for example Tim-4 and MFG-E8 (52) develop autoimmunity at an earlier age, or triple knockout of TAM (Tyro3, Axl, and Mer) (35) have a more potent onset of disease than Mer alone), collectively these data suggest, at least in the mouse, that PS receptors are not functionally redundant. This evidence concerns the gene MERTK and Autoimmunity.