In the present study, FCN1 and MASP2 were up-regulated 4- and 2.8-fold, respectively, in pre- compared with post-splenectomy serum, suggesting that uncontrolled non-regenerative anemia with complement activation may be relevant to the immune-mediated destruction of erythroid progenitor cells, which has been considered as a pathophysiology of PIMA [6]. The gene discussed is MASP2; the disease is anemia.