Similar to Hem-1–deficient children, Hem-1–null mice exhibited membranous glomerulopathy (23), a disease often associated with autoantibody production; increased expression of the acute phase proteins serum amyloid A1 (SAA1), SAA2, and SAA3; splenomegaly; anemia; liver calcification (due to amyloid deposition); and diffuse inflammation in multiple tissues including epididymis, mesentery, heart, and lungs (23, 24). This evidence concerns the gene SAA2 and anemia.