We found that exposure of Kasumi-1 and MV4-11 cells to TQ led to downregulation of KIT, FLT3, STAT5 and AKT followed by dephosphorylation of STAT5 and AKT (Figure 2E), indicating tyrosine kinase signaling as an additional molecular mechanism behind TQ-induced leukemia growth arrest, which merits a systematic characterization. Here, AKT1 is linked to leukemia.