Analysis of pathology revealed correction of characteristic sickle pathology in mice that received transplants. The 4 columns (from left to right) show microscopic findings in the sickle controls (panels A,E,I,M,Q), a representative mouse that received a transplant with less than 50% RBC chimerism (panels B,F,N,R [mouse no. 1582], J [mouse no. 1550]), a representative mouse that received a transplant with more than 70% to 80% RBC chimerism (panels C,G,K,O,S [mouse no. 70]) and a healthy eGFP control (panels D,H,L,P,T). The 5 rows (top to bottom) show sections of cardiac medium-sized arteries (panels A-D; hematoxylin and eosin [H&E] original magnification × 100), sections of a wall of a pulmonary artery (panels E-H: H&E stain; original magnification × 400), representative hepatic section (panels I-L: H&E stain; original magnification × 400) with iron stain inset (original magnification, × 400), representative renal section (panels M-P: trichrome stain; original magnification × 100) with iron stain inset (original magnification, × 400), and representative spleen section (panels Q-T: H&E stain; original magnification × 100). For the sickle controls and mice with less than 50% RBC chimerism, the figure illustrates ectasia of cardiac medium-sized arteries; increased thickness of the media of the pulmonary artery; hepatic infarcts; severe iron deposition in hepatocytes, hepatic Kupffer cells, and hepatic histiocytic cells; cortical renal infarcts with chronic inflammatory infiltrates; severe deposition of iron in renal tubular epithelium; and loss of splenic architecture with increased hematopoietic cells, ectasia of medium-sized arteries, and sinusoidal congestion. Mice that received transplants with more than 70% to 80% RBC chimerism showed changes intermediate between the healthy eGFP control and sickle control in the cardiac vascular ectasia, pulmonary artery wall thickness, and hepatic and renal tubular iron deposition. They showed no recent hepatic or renal infarcts, they demonstrated fibrosis consistent with remote infarcts, and they showed some return of the normal nodular architecture of the splenic white pulp.