Using this technique, Behbehani et al. observed that the expression of several surface markers (e.g., CD7, CD33, CD34, CD38, CD45, CD47, CD71, CD99, CD117, CD123, CD321, HLA-DR) on Lin-CD34+CD38lo LSC varied according to AML genetic signature and karyotype and that different AML subtypes were associated with distinct intracellular signaling in LSC [43]. The gene discussed is CD99; the disease is acute myeloid leukemia.