Our adoptive transfer studies effectively ruled out autoimmunity as the trigger for increased platelet turnover in Rasa3-mutant mice, and R3hlb/hlb platelets did not exhibit increased exposure of galactosyl (β-1,4) N-acetylglucosamine (Galβ4GlcNAc) (Erythrina cristagalli lectin, ECL) or galactosyl (β-1,3) N-acetylgalactosamine (Galβ3GalNAc) (peanut agglutinin, PNA) residues (Figure 4A; ref. 29). The gene discussed is RASA3; the disease is Autoimmunity.