EPHB4 expression is driven by mutations found in AML. (A) Treatment with inhibitor of BCR-ABL (imatinib) led to a decrease of EPHB4 expression on the surface of bcr-ABL–containing K562 cells lines, with no change in ML-2 cells, which had wild-type (wt) ABL. (B) Treatment with the specific FLT3 inhibitor, quizartinib led to a decrease of EPHB4 expression in FLT3-ITD–containing MV-4-11 and MOLM-14 cells, but no change in FLT3-wt cells. (C) Treatment with the JAK inhibitor ruxolitinib resulted in a decrease of EPHB4 expression on JAK2V617F-containing HEL cells, with no change in JAK2-wt controls.