Using signal-sequence-trap technology to identify surface antigen expression milieu, followed by quantitative real-time polymerase chain reaction (qRT-PCR) validation across Lin−CD34+CD38− AML samples and normal BM-derived HSC/progenitor cells, Hosen and coworkers found CD96 to be preferentially upregulated in AML cells and demonstrated LSC activity among CD34+CD38−CD96+ AML cells through successful engraftment of these cells into irradiated immunocompromised mice [29]. The gene discussed is CD38; the disease is acute myeloid leukemia.