To better understand the mechanisms behind the delay in leukemia progression observed with Selplg–/– AML, a parallel cohort of mice was sacrificed at 3 weeks post-transplant for analysis of the body distribution of AML blasts [characterization of the total number of AML blasts in the BM, blood and spleen of a leukemic mouse as described previously (Winkler et al., 2013)]. The gene discussed is SELPLG; the disease is acute myeloid leukemia.