We hypothesize that hemolytic anemia during HUS, by definition the loss of erythrocytes due to their mechanical deformation and disruption in the bloodstream, arises not only from intravascular cell damage due to passing through occluded microvessels, but also from the extravascular impairment of erythrocyte progenitors in the bone marrow via direct damage by Stx2a leading to “non-hemolytic” anemia. This evidence concerns the gene STX2 and hemolytic-uremic syndrome.