TLR9 on the surface of RBCs could bind to free DNA derived from mitochondria, bacteria and plasmodia.59 The DNA-bound RBCs lose normal morphology and function, promoting RBCs clearance by splenic macrophages and causing acute anemia in a TLR9-dependent manner.59 Septic patients with anemia are characterized by increased levels of RBC-associated mtDNA compared with septic patients without anemia.59 Here, TLR9 is linked to anemia (phenotype).