However, we failed to show consistently increased active RAS-GTP in hlb381 erythroid cells, indicating that absence of RASA3 does not significantly alter RAS activation and perhaps accounting, at least in part, for the absence of significant anemia in hlb381. The data in total suggest that mechanisms in addition to failure of mutant RASA3 to bind the membrane in scat cells and/or currently unknown compensatory mechanisms due to genetic modifiers operating in hlb381 influence hematopoiesis in mouse models of Rasa3 defects. Here, RASA3 is linked to anemia.