By longitudinal scRNA-seq of 6 AML patients during cytarabine (Ara-c)-based treatment, upregulation of CD52 and LGALS1 (the marker for QSC phenotype) was observed, where CD52-SIGLEC10 interaction between QSCs and monocytes may underly the mechanism for immune evasion and resistance [104]. This evidence concerns the gene CD52 and acute myeloid leukemia.